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PHASE 2A (Mine) > RESP > Flashcards

RESP Flashcards

1
Q

What is FEV1?

A

The force expiratory volume in 1 second (Max inspiration followed by max exparation)

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2
Q

How much of the vital capacity can healthy individuals expire in 1 seconds?

A

80% of vital capacity

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3
Q

What is vital capacity?

A

The maximal volume of air that can be expired following maximum inspiration

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4
Q

What is inspiratory reserve volume?

A

The amount of air that can be inhaled above tidal volume during a forceful breath in.

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5
Q

What is tidal volume?

A

The amount of air that moves in and out of the lungs with each respiratory cycle

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6
Q

What is functional residual capacity?

A

The amount of air remianing in the lungs at the end of a normal exhalation

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7
Q

What is residual volume?

A

The volume of air remaining in the lungs after maximum forceful expiration

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8
Q

What is expiratory reserve volume?

A

The volume of air, above normal tidal volume that can be exhaled during a forceful breath out

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9
Q

What is vital lung capacity?

A

The maximum amount of air you can forcibly exhale after fully inhaling.

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10
Q

What is the average tidal volume?

A

500ml male

400ml female

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11
Q

What is FVC?

A

Forced vital capacity–> The total amount of air forcibly expired.

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12
Q

What is an FEV1 or FVC result compared with?

A

The predicted value for that patient: if it’s 80% or greater than the predicted value then the result is normal.

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13
Q

What is the different between the FEV1 and FVC test?

A

FEV1 is the forced expiratory volume in 1 second, whereas FVC is the full amount of air that can be exhaled in a complete breath

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14
Q

Which test is better (FEV1/ FVC) and why?

A

FEV1 is more reproducible

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15
Q

What does a low FVC indicate?

A

Airways restriction

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16
Q

What is the FEV1/ FVC ratio?

A

The proportion of FVC exhaled in the 1st second

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17
Q

What does it indicate the if the FEV1/ FVC ratio is below 0.7?

A

Airways obstruction

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18
Q

Why does a low FEV1/FVC ratio indicate airway obstruction?

A

The FEV1 is reduced due to the obstruction but the overall capacity doesn’t change

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19
Q

What does a normal/ high FEV1/FVC ratio with low FVC (and FEV1) percentages (<80%) indicate?

A

Airways restriction

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20
Q

Why does a high FEV1/ FVC ratio indicate airway restriction?

A

Easy for them to breathe out quickly but low FVC as they can’t exhale fully

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21
Q

Which of inspiration and expiration is an active process?

A

Inspiration

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22
Q

What structures does air move through to get to the lungs and what are the two zones?

A

Conducting airway:
Trachea–> Main bronchi–> Lobar bronchi–> Segmental bronchi–> Terminal bronchioles
Respiratory airway:
Respiratory bronchioles–> Alveolar duct–> alveolar sac

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23
Q

What happens during inspiration?

A

The diaphragm contracts and flattens and the external intercostal muscles elevate the ribs and sternum.
The volume increases and pressure decreases, meaning the environmental pressure is now greater so air rushes in down a pressure gradient

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24
Q

What happens during expiration?

A

Relaxation of the diaphragm and external intercostal muscles, decreasing the volume of the thoracic cavity and increasing the pressure, forcing air to move out.

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25
Q

What is airways obstruction and what are the main causes?

A

When the lungs are unable to expel air properly during exhalation:
COPD, asthma, cystic fibrosis

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26
Q

What is airways restriction and what are the main causes?

A

When the lungs are unable to fully expand, limiting the amount of O2 taking in:
Pulmonary fibrosis, sarcoid

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27
Q

What is type 1 respiratory failure?

A

Low oxygen levels in the blood (hypoxaemia) with either a normal or low CO2 level.

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28
Q

What is type 2 respiratory failure?

A

Low oxygen levels with high carbon dioxide. (2 changes–> low pO2 + high CO2)

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29
Q

What is the most common cause of type 1 respiratory failure?

A

Pulmonary embolism (that causes a V/Q mismatch)

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30
Q

What is the most common cause of type 2 respiratory failure?

A

Hypoventilation

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31
Q

What is V/Q mismatch?

A

When part of the lung receives oxygen without blood flow or vice versa (there is blood flow without oxygen.)

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32
Q

What causes Type 1 respiratory failure?

A 
The lungs being unable to meet the demands of the body due to: 
V/Q mismatch
High altitude
Shunting
Asthma
Pneumonia
Diffusion impairment
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33
Q

Why does high altitude cause type 1 respiratory failure?

A

Low oxygen levels

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34
Q

What is shunting and why does it cause type 1 respiratory failure?

A

When a hole in the heart

means that deoxygenated blood can mix with oxygenated, reducing the overall pressure of O2 in the blood

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35
Q

What is diffusion impairment?

A

When O2 is not able to diffuse into the blood

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36
Q

What causes Type 2 respiratory failure?

A 
Pump failure so that CO2 can't be removed quick enough and/or O2 cannot arrive at tissues quick enough (poor ventilation) caused by: 
Depressed central respiratory drive
Neuromuscular dysfunction
Mechanical defect
COPD 
asthma
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37
Q

What is the name for increased CO2 in the blood?

A

Hypercapnia

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38
Q

What are the signs of hypercapnoea?

A 
Racing pulse
Flapping tremor
Confusion
Drowsiness
Reduced consciousness
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39
Q

What is the transfer co-efficienct?

A

The measure of the ability of oxygen to diffuse across the alveolar membrane

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40
Q

How is the transfer co-efficient calculated?

A

By inspiring a small amount of CO, holding breath for 10 seconds at total lung capacity and measuring the amount of gas transfered.

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41
Q

What test is used to measure lung function?

A

Spirometry

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42
Q

What does spirometry involve?

A

Different breathing exercises into a machine that measures volumes of air and flow rates.

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43
Q

What is reversibility testing?

A

Giving a bronchodilator (salbutamol) prior to repeating spirometry to see the impact it has on results

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44
Q

What is peak flow?

A

Measure of the fastest point of a persons expiratory flow of air.

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45
Q

How is peak flow measured?

A

Peak flow meter–> stand tall, take deep breath in, make a good seal around the device and blow as fast and hard as possible. Repeat 3 times.

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46
Q

When is peak flow useful?

A

In obstructive lung disease (e.g. asthma) to see how well it is controlled and how sever an acute exacerbation is.

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47
Q

What is COPD?

A

Chronic obstructive pulmonary disease: non-reversible, long term deterioration in air flow through the lungs caused by damage to lung tissue.

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48
Q

What is the most common cause of lung damage in COPD?

A

Smoking

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49
Q

What triggers exacerbations of COPD? (worsening of lung function)

A

Infections

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50
Q

What is the typical presentation of suspected COPD?

A 
Long term smoker presenting with:
Chronic shortness of breath
Cough
Sputum production
Wheeze 
Recurrent respiratory infections.
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51
Q

What other diagnoses should be considered during a COPD diagnosis?

A

Lung cancer, fibrosis, heart failure

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52
Q

How is breathlessness assessed?

A

MRC Dyspnoea scale:
Grade 1: Breathless on strenuous exercise
Grade 2: Breathless on walking up hill
Grade 3: breathless that slows walking on the flat
Grade 4: Stop to catch breath after walking 100 metres
Grade 5: Unable to leave house due to breathlessness

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53
Q

How is COPD diagnosed?

A

Clinical presentation + Spirometry

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54
Q

What will spirometry show in a patient with COPD?

A

An obstructive picture: Overall lung capacity is not as bad as their ability to quickly blow air out of the lungs.

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55
Q

What will the FEV1/FVC ratio look like in COPD?

A

<0.7 as it is obstructive. (Low FEV1)

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56
Q

How is the severity of airflow obstruction graded?

A 
Using FEV1-->
Stage 1: >80% of predicted
Stage 2: 50-79% 
Stage 3: 30-49%
Stage 4: <30%
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57
Q

What investigations other than spirometry can help with diagnosis/ management of COPD?

A 
CXR (excludes cancer)
FBC (for polycythamia/ anaemia) 
BMI (to check changes in future)
Sputum culture (to assess for infection) 
ECG/ Echo (assess heart function) 
CT thorax (to check for alternate diagnosis)
Serum alpha-1 antitrypsin
TLCO
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58
Q

What is TLCO and what happens to its levels in COPD?

A

Transfer factor for carbon monoxide–> decreased in COPD.

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59
Q

What is the essential management of COPD to prevent it getting worse?

A

Stop smoking

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60
Q

What is the first step in COPD treatment?

A

Short acting bronchodilator inhalers:

Beta-2 agonists or antimuscarinics

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61
Q

What are the most commonly used short acting bronchodilators?

A

Salbutamol or terbutaline (beta-2 agonists)

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62
Q

What is the action of beta-2 agonists?

A

Act directly on beta-2 receptors, causing smooth muscle relaxation and dilation of the airways.

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63
Q

What are antimuscarinics?

A

Block acetylcholine at muscarnic receptor sites, causing bronchodilation

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64
Q

When should short acting inhalers be used and how often can they be?

A

Should be used when you feel breathless, up to 4 times a day.

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65
Q

How quickly do short-acting bronchodilators work and how long do they last?

A

Usually within a few minutes, and last 4-5 hours

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66
Q

When would you move on to step 2 of COPD treatment?

A

If the patient is experiencing symptoms regularly throughout the day

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67
Q

What is the second step in COPD management?

A

Long-acting bronchodilators

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68
Q

What are the 2 types of long acting bronchodilators (with examples) and how long do they last?

A

LABA: Beta-2 antagonists (salmeterol, formoterol)
LAMA: Antimuscarinics (Tiotropium)

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69
Q

What would be added if a patient on a long acting bronchodilator was still becoming breathless or having frequent flare ups?

A

A steroid inhaler- usually in a combination inhaler with a long-acting medicine

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70
Q

What is the action of steroid inhalers ?

A

Reduced inflammation in the airways

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71
Q

What is the 4th line in COPD managment?

A

Trio inhaler: LABA, LAMA and ICS (Inhaled corticosteroid) combination

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72
Q

What other medications can be added in severe cases of COPD?

A 
Nebulisers
Oral theophylline
Oral mucolytic therapy (breaks down sputum)
Long term prophylactic antibiotics
Long term home oxygen therapy
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73
Q

What is a nebuliser?

A

A machine that helps you breathe in a medicine through a mask or mouthpiece

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74
Q

When is long term home oxygen therapy used ?

A

In severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension.

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75
Q

How does an exacerbation of COPD present?

A

Acute worsening of symptoms such as cough, SOB, sputum production and wheeze

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76
Q

How does CO2 make the blood acidotic?

A

Breaks down into carbonic acid.

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77
Q

What does a low pH with a raised pCO2 indicate is happening in the body?

A

Respiratory acidosis: They are acutely retaining (not able to get rid of CO2)

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78
Q

What does raised bicarbonate in the blood indicate?

A

Chronic retention of CO2

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79
Q

Why is there raised bicarbonate in chronic CO2 retention?

A

Because the kidneys respond to high levels of CO2 by producing more bicarbonate to maintain normal pH.

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80
Q

What happens to the acid levels in an acute COPD exacerbation?

A

The kidneys can’t keep up with rising levels of CO2 so the patient becomes acidotic despite having higher bicarbonate than normal.

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81
Q

What test would be done to check pO2, pCO2 and bicarbonate levels?

A

ABG

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82
Q

What are the two main COPD diseases?

A

Chronic bronchitis
Emphysema
(usually both)

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83
Q

What is emphysema?

A

Damage to the alveoli, causing loss of elastic recoil, with collapse of the small airways during expiration and enlarged air spaces.

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84
Q

What is usually the cause of early onset COPD?

A

Alpha-1 antitrypsin deficiency

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85
Q

What is Alpha-1 antitrypsin deficiency?

A

Condition caused by an abnormality in the gene for the protease inhibitor alpha-1-antitrypsin

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86
Q

What is the pathophysiology of alpha-1 antitrypsin deficiency?

A

Elastase is an enzyme secreted by neutrophils that digests connective tissues. Alpha-1-antitrypsin is protein produced in the liver that offers protection from elastase enzyme. In deficiency, the protection is no longer there so elastase can digest connective tissue

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87
Q

What is the cause of alpha-1 antitrypsin deficiency?

A

Autosomal recessive defect in the gene for A1T1 on chromosome 14

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88
Q

What are the two main organs affected by alpha-1 antitrypsin deficiency and what does it cause?

A

Liver–> Liver cirrhosis

Lungs–> Bronchiectasis and emphysema (COPD)

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89
Q

What is bronchiectasis?

A

Long term condition where the airways become abnormally widened, leading to excess mucus build up that can make the lungs more vulnerable to infection

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90
Q

What happens to the lung in the lack of a normal, functioning alpha-1-antitrypsin protein?

A

Excess protease enzymes attack the connective tissue leading to COPD (bronchiectasis and emphysema.)

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91
Q

How is alpha-1 antitrypsin deficiency diagnosed?

A

Low serum-alpha-1-antitrypsin
Liver biopsy
Genetic testing
High resolution CT thorax

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92
Q

What is chronic bronchitis?

A

Infection of the bronchi, causing them to become irritated and inflamed, and resulting in excess mucus production

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93
Q

How is chronic bronchitis classified?

A

Daily productive cough that lasts for 3 months of the year, and for at least 2 years in a row

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94
Q

What is the epithelium of the respiratory tract?

A

Ciliated, pseudostratified columnar epithelium with goblet cells.

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95
Q

What is underneath the epithelium?

A

Lamina propria:
Basement membrane
Loose connective tissue

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96
Q

What is the mucosa and what is it composed of?

A

The membrane lining the respiratory tract:

Epithelium + Lamina propria (basement membrane, loose connective tissue)

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97
Q

What is underneath the mucosa and what does it consist of?

A

Submucosa:
Smooth muscle
Connective tissue

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98
Q

Where are the bronchial mucinous glands located and what do they do?

A

In the submucosa

Secrete the majority of the mucus in the lumen of the bronchi

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99
Q

What layer is in the bronchi but not the bronchioles (underneath the submucosa)?

A

Layer of cartilage

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100
Q

What does exposure to irritants/ chemicals (e.g. smoking) do to mucus production and why?

A

Causes hypertrophy and hyperplasia of the bronchial mucinous glands in the bronchi, and goblet cells in the bronchioles increasing mucus production

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101
Q

Why is even a small increase in mucus a problem in the bronchioles?

A

It causes obstruction, leading to air trapping

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102
Q

What does smoking do to cilia?

A

Makes them shorter and less mobile, meaning its harder for them to move mucus

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103
Q

Why do people with bronchitis have a productive cough?

A

There is excess mucus and reduced cilia function, meaning they have to rely on coughing to move mucus plugs.

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104
Q

Why do patients with chronic bronchitis wheeze?

A

Due to narrowing of the passageway for the air to move in and out

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105
Q

Why do patients with chronic bronchitis have crackles (Rales)?

A

Caused by popping open of small airways

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106
Q

Why is there hypoxemia and hypercapnia in chronic bronchitis?

A

Mucus plugs block airflow, increasing the pCO2. This decreases pO2, meaning less oxygen gets to the blood and makes it harder for CO2 to get out of the blood.

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107
Q

What can increased CO2 levels in the blood called?

A

Cyanosis- blue discolouration of skin

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108
Q

What can patients with chronic bronchitis be referred as and why?

A

Blue bloaters:

as they may get cyanosis due to high CO2 levels.

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109
Q

What do blood vessels do in response to poor ventilation?

A

Vasoconstrict to try and move blood to somewhere where there is better ventilation- doesn’t work when large portion of the lung is affected

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110
Q

What does vasoconstriction of a large proportion of the lung lead to?

A

Increased pulmonary vascular resistance, leading to pulmonary hypertension

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111
Q

What can pulmonary hypertension cause

A

Right sided heart failure:

Cor pulmonale

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112
Q

What can mucus plugging in the airways also cause?

A

Lung infections behind the blockages

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113
Q

What damage to irritants (e.g. cigarette smoke) cause in emphysema?

A

Trigger an inflammatory reaction, attracting immune cells to the alveoli.

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114
Q

What do immune cells release that damage the alveoli in emphysema?

A

Release inflammatory chemicals and proteases (elastases and collegeaenases)

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115
Q

What is Bernoulli’s principle?

A

That air moving at high velocity must be at low pressure

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116
Q

What does loss of elastin do to the alveoli?

A

Weakens the walls, allowing them to be pulled inwards and collapse during exhalation.
Also makes them more compliant, so they expand and hold air in during inhalation.
Causes breakdown of septa, meaning alveoli merge to form large air spaces.

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117
Q

What does the loss of septa (alveolar walls) cause?

A

Neighbouring alveoli to merge and form a large air space, reducing the available surface for gas exchange.

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118
Q

Why does emphysema cause shortness of breath?

A

Because there is decreased gas exchange due to air trapping and reduced surface area.

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119
Q

What are emphysema patients sometimes referred to as and why?

A

Pink puffers:
Often exhale slowly through pursed lips to increase the pressure in the airways and stop them collapsing. Pink because they are oxygenated.

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120
Q

What symptoms occur after prolonged emphysema?

A

Hypoxemia
Cough (with some spitum caused by inflammation of bronchioles)
Barrel shaped chest

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121
Q

What are the X-ray findings in a patient with emphysema?

A

Increased anterior-posterior diameter
Increased lung field lucency
Flattened diaphragm

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122
Q

What are the 3 types of emphysema?

A

Centriacinar
Panacinar
Paraseptal

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123
Q

What is centriacinar emphysema and what is the most common cause?

A

Damage to the central/ proximal alveoli. Most common in smoking as smoke is not able to reach the most distal alveoli

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124
Q

What is panacinar emphysema and what is the most common cause?

A

Entire acinus is affected. Usually caused by alpha-1-antitrypsin deficiency

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125
Q

What is paraseptal emphysema and what can it cause?

A

Emphysema affecting the distal alveoli on the peripheries of the lungs. If these rupture, it can cause a pneomothroax.

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126
Q

Why does alpha-1-antitrypsin cause emphysema?

A

Elastase damages the elastin (as alpha-1-antitrypsin isn’t there to stop it) and so the alveolar walls are damages and collapse.

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127
Q

What do the blood vessels of the lungs do to try to counteract the poor ventilation and why doesn’t this work?

A

Vasoconstrict to try to divert the blood to somewhere with better ventilation, but the majority of the lung is affected so it doesn’t work

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128
Q

What can COPD do to the heart and how?

A

Cause Cor Pulmonale: right sided heart failure as the lungs vasoconstrict, leading to pulmonary hypertension.

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129
Q

What does the loss of elastic recoil in emphysema cause?

A

Expiratory airflow limitation and air trapping

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130
Q

What is the most common form of emphysema?

A

Centri-acinar emphysema

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131
Q

What does the combination of emphysema and chronic bronchitis lead to?

A

Severe airflow limitation

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132
Q

What are the causes of V/Q mismatch in COPD?

A

Air trapping: Caused by mucus plugging/ rapid collapse during expiration.
Small airways

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133
Q

What type of respiratory failure does COPD cause?

A

Both types (more commonly type 2)

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134
Q

What are the main signs and symptoms of COPD?

A

Dyspnoea, tachypnoea, barrel chest, SOB, chronic cough, recurrent chest infection.

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135
Q

Why is excess oxygen a bad idea when treating a COPD excacerbation?

A

It can depress their respiratory drive, slowing down the breathing rate and effort, leading to more CO2 retention.

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136
Q

How is oxygen given to treat COPD and under guidance from what?

A

Given through venturi masks (designed to deliver specific percentage concentration of oxygen) under the guidance of oxygen saturations and repeat ABG’s to ensure the optimum pO2 without increasing pCO2.

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137
Q

What is the target oxygen saturations in a patient retatining CO2?

A

88-92%

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138
Q

What is the target oxygen saturation in a patient not retaining Co2 with normal bicarb?

A

> 94%

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139
Q

How is a COPD exacerbation treated at home?

A

Prednisolone - anti-inflammatory (30mg o.d. 7-14 days)
Regular inhalers/ nebulisers
Antibiotics if signs of infection

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140
Q

How is a COPD exacerbation treated in hospital?

A

Nebulised bronchodilators (e.g. salbutamol, ipratropium)
Steroids
Antibiotics
Physiotherapy to clear sputum

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141
Q

What are the COPD treatment options in severe exacerbations not responding to first line treatment?

A

IV aminophylline
Non-invasive ventilation
Intubation/ ventilation
Doxapram (resp stimulant)

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142
Q

What is asthma?

A

Chronic inflammation of the airways that causes episodic exacerbations of bronchoconstriction

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143
Q

Does asthma cause airways restriction or airways obstruction?

A

Airways obstruction (caused by narrowing of airways)

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144
Q

What causes bronchoconstriction in asthma?

A

hypersensitivity of the airways (usually triggered by environmental factors)

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145
Q

What type of hypersensitivity reaction is asthma?

A

Type 1

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146
Q

What happens in a type 1 hypersensitivity reaction?

A

IgE mediated immediate hypersensitivity triggered by re-exposure to a specific allergen.

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147
Q

What are some allergens that trigger asthma?

A 
Air pollution (smoke, car exhaust)
Dust
Pollen 
Animal hair
Mites
Mould
Medications (aspirin)
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148
Q

What happens on subsequent exposure to an allergen in asthma?

A

The allergen binds to primed mast cells, stimulating them to degranulate and release pro-inflammatory mediators which cause an allergic reaction.

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149
Q

What is the main pro-inflammatory mediator and what is its action?

A

Histamine:

  • Binds to H1 receptors on smooth muscle and causes bronchoconstriction
  • Causes blood vessel dilation and increased permeability of cell walls, increasing blood flow to the area but also causing fluid to leak into the interstitium, causing oedema and urtica (hives)
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150
Q

What are the typical triggers of bronchoconstriction in asthma?

A 
Infection
Night/ early morning
Exercise
Animals
Cold/ damp
Dust
Strong emotions
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151
Q

What happens when you come into contact with a trigger in asthma?

A

The hypersensitivity reaction causes smooth muscle spasms and increased mucus secretion, resulting in narrowing of the airways.

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152
Q

What happens after many years of having asthma?

A

Irreversible changes begin to take place–> permenant narrowing of the airways.

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153
Q

What are the key presentations of asthma?

A 
Episodic symptoms which are typically worse at night.
Dyspnoea
Dry cough
Chest tightness
Wheezing
Sputum
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154
Q

What do patients with asthma also commonly have?

A

Other atopic conditions: eczema, hayfever, food allergies

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155
Q

How is asthma diagnosed?

A

Clinical diagnosis based on history/ effectiveness of treatment
Fractional exhaled nitric oxide test (FeNO)
Spirometry
Peak flow test

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156
Q

In what different ways can asthma be classified?

A

Frequency of symptoms
FEV1
PEFR
Frequency of medication use

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157
Q

What is the stepwise process by which asthma managed?

A
  1. SABA (blue reliever inhaler)
  2. SABA + ICS (reliever + brown preventer inhaler)
  3. SABA + ICS + LABA/ LAMA
    • Leukotriene receptor antagonist/ MART inhaler
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158
Q

What are the symptoms of an acute asthma attack?

A

Progressively worse shortening of breath
Tachypnoea
Use of accessory muscles
Symmetrical expiratory wheeze and tight chest sounds

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159
Q 
What is the PEFR in a:
- Moderate
-Severe
-Life threatening
asthma attack?
A

M: 50-75% of predicted
S: 33-50% of predicted
Life threatening: <33% predicted

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160
Q

What are the stats in a severe asthma attack?

A

PEFR 33-50%
Resp rate >25
Heart rate >110
Unable to complete sentences

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161
Q

How do you know it is a life threatening asthma attack?

A

Oxygen saturation <92%
No wheeze (silent chest: no air entry at all)
Confusion/ exhaustion
Haemodynamic instability (shock)

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162
Q

How is a severe acute asthma attack treated?

A 
Oxygen therapy to maintain O2 sats
Nebulised salbutamol
Prednisolone
Aminophylline
Magnesium sulphate infusion
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163
Q

How are sever asthma attacks monitored?

A 
ABGs
Respiratory rate
Respiratory effort
Peak flow
Oxygen sats
Chest auscultation
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164
Q

What is bronchiectasis?

A

Chronic inflammation of the bronchi and bronchioles, leading to permenant dilation of the airways.

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165
Q

What are the main causes of bronchiectasis?

A

Post infection (pneumonia, whooping cough, TB e.t.c.)
Ciliary dysfunction (Ciliary dyskinesia)
Cystic fibrosis
Airway obstruction (e.g. tumour, foreign body)
Allergic bronchopulonary aspergillosis

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166
Q

What happens in bronchioectasis?

A

The mucociliary elevators malfunctions, leading to mucus plugs forming. This allows bacteria to multiply and cause infection, damaging the bronchi and causing them to dilate and more mucus to be present, making it more vulnerable to infection. (viscious cycle)

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167
Q

What does chronic infection do to bronchi walls?

A

Causes immune cells to release cytokines that damage the ciliated epithelial cells and destroy the elastin in the walls, meaning over time they become dilated and filled with mucus.

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168
Q

Why does fibrosis occur in bronchioectasis?

A

Fibroblasts enter to try and repair the damage, depositing collagen which in the absence of elastin, makes the lungs stiff.

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169
Q

What are the key presentations of bronchiectasis?

A

Productive cough (lots of smelly mucus)
Shortness of breath
Wheezing

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170
Q

How is bronchiectasis diagnosed?

A

HRCT–> dilated bronchi

Lung function test (indicated obstruction)

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171
Q

How is bronchiectasis managed?

A

Infection treated with antibiotics
Postural drainage of excess mucus
Surgery to remove obstruction

172
Q

What is cystic fibrosis?

A

Autosomal recessive genetic condition affecting mucus glands.

173
Q

What causes cystic fibrosis?

A

Autosomal recessive genetic mutation of cystic fibrosis transmembrane conductance regulatory gene on chromosome 7

174
Q

How many people are carriers of the CF mutuation?

A

1 in 25

175
Q

What are the three main consequences of cystic fibrosis? (3 places it affects)

A
  1. Mucus blocks pancreatic ducts, resulting in lack of digestive enzymes reaching to small intestine
  2. Thick airway secretions reduce airway clearance, resulting in infections.
  3. Congenital absence of the vas deferens in males leads to infertility.
176
Q

What is usually the first sign of cystic fibrosis? (20% patients)

A

Meconium ileus–> When the first stool a baby passes is so thick and sticky, it gets stuck in the intestine.

177
Q

What are the typical signs of CF in childhood?

A

Recurrent lower resp tract infections
Failure to thrice
Pancreatitis

178
Q

What are the main symptoms of CF?

A 
Chronic cough
Thick sputum production
Recurrent infections
Steatorrhoea (loose, greasy stools)
Abdominal pain/ bloating
Salty skin
179
Q

What are the main signs of CF?

A 
Failure to thrive (low weight/ height)
Nasal polyps
Finger clubbing
Crackles/ wheezes on auscultation 
Abdominal distention
180
Q

How is cystic fibrosis diagnosed?

A

Screening of newborns
Sweat test (GOLD STANDARD)
Genetic testing

181
Q

What does the newborn screening test look for>

A

IRT pancreatic enzyme that is released when the pancreas is damaged

182
Q

What is the sweat test and what level indicates CF?

A

Pilocarpine applied to patch of skin, electrodes are places either side and a current is passed to stimulate sweat. The sweat is absorbed with gauze and sent to the lab to test chloride concentration. > 60mmol/L Cl is diagnostic.

183
Q

Why is there excess chloride in sweat in CF?

A

Because the mutation affects the protein channels that transport chloride, meaning it can’t enter.

184
Q

What are the main bacterial colonisers in CF?

A

Staph. aureus

Pseudomomas aeruginosa

185
Q

Which bacteria has the worst prognosis if colonised in CF and why?

A

Pseudomonas-> Is resistant to multiple antibiotics and leads to significant increase in morbidity and mortality.

186
Q

What are the different aspects to CF management?

A

Physiotherapy to clear mucus
Nutrition
Medication

187
Q

What nutrition management is used for patients with CF?

A

High calorie diet
CREON tablets to digest fats (replace pancreatic enzymes)
Fat soluble vitamins given

188
Q

What medication can be given to aid CF management?

A

Prophylactic flucloxacillin
Bronchodilators (salbutamol)
Vaccinations
Nebulised mucus thinners (DNase)

189
Q

What are treatment options for severe complications of CF?

A

Lung transplant
Liver transplant
Fertility treatment for infertile males
Genetic counselling

190
Q

How are CF patients monitored and how frequently?

A

Seen in specialist clinics every 6 months. Regular monitoring of sputum for colonising bacteria, screening for other conditions, pulmonary function tests.

191
Q

What other conditions may occur as a result of CF?

A

Diabetes, osteoporosis, vitamin D deficiency, liver failure.

192
Q

What does CF prognosis depend on?

A
  • Severity of symptoms
  • Type of mutation
  • Adherence to treatment
  • Frequency of infection
  • Lifestyle
193
Q

What is the prognosis of CF?

A 
Life expectancy 47 years
90% develop pancreatic insufficiency
50% develop diabetes
30% develop liver disease 
Most males are infertile
194
Q

What are restrictive lung diseases?

A

When the lungs are unable to fully expand, limiting the amount of oxygen intake during inhalation

195
Q

What are the two types of restrictive lung disease?

A

Interstitial lung disease

Extra-pulmonary

196
Q

What is interstitial lung disease?

A

Conditions that affect the lung parenchyma (tissue), causing inflammation and fibrosis

197
Q

What is between the alveoli of the lungs?

A

Connective tissue made up of elastin and collagen

198
Q

How is interstitial lung disease generally diagnosed?

A

Clinical features + HRCT (shows ‘ground glass’ appearance) + Lung biopsy

199
Q

How is interstitial lung disease generally managed?

A 
Poor prognosis/ limited options
Supportive treatment:
-Remove/ treat underlying cause
-Home oxygen
-Stop smoking
-Physio
-Vaccine
-Lung transplant in limited cases
200
Q

What happens to healthy lung tissue in interstitial lung disease?

A

It is replaced by fibrosis, making the lungs stiff and unable to expand.

201
Q 
What happens to the 
-Total lung capacity
-FEV1
-FEV
in interstitial lung disease?
A

All decrease

202
Q

What happens to the FEV1:FVC ratio in restrictive lung disease?

A

Stays the same or increases (provides elastic recoil which pushes air out faster)

203
Q

What are the different types of interstitial lung disease?

A
  • Pulmonary fibrosis (Idiopathic, drug induced, secondary)
  • Sarcoidosis
  • Hypersensitivity pneumonitis
  • Occupational lung disorders (pneumoconiosis)
  • Cryptogenic organising pneumonia
204
Q

What is sarcoidosis?

A

Granulomatoues inflammatory condition causing restrictive fibrosis of the lungs

205
Q

What is the typical presenting patient with sarcoidosis?

A

Young african american woman presenting with a cough

206
Q

What happens in sarcoidosis?

A

Unknown mechanisms causes immune cells to surround a pathogen instead of destroy it, forming granulomas which accumulate in the body, particularly the lymph nodes.

207
Q

Which parts of the body are particularly affected by sarcoidosis?

A
  • Lungs (90%)
  • Liver (20%)
  • Eyes (20%)
  • Skin (15%)
  • Heart (5%)
  • Kidneys (5%)
  • CNS (5%)
208
Q

Which area is most affected by granulomas in sarcoidosis?

A

Hilum of the lungs causing bilateral hilar lymphadenopathy

209
Q

What other things may be present in sarcoidosis?

A 
Erythema nodosum (fat nodules on skin) 
Polyarthralgia
Uveitis
Arrhythmias
etc
210
Q

What are the key presentations of sarcoidosis?

A

50% asymptomatic
Dry cough
S.O.B
Systemic symptoms (fever, fatigue, weight loss)

211
Q

How is sarcoidosis diagnosed?

A

Biopsy
Blood tests
Imaging (CXR, HRCT)

212
Q

What will a biopsy show in sarcoidosis?

A

non-caseating (no necrosis) granulomas

213
Q

How is sarcoidosis managed?

A

No treatment for mild cases- will clear up on its own

Oral steroids in severe cases

214
Q

What is idiopathic pulmonary fibrosis?

A

Restricted lung disease caused by idiopathic, progressive fibrosis of the interstitium.

215
Q

What are the risk factors in idiopathic pulmonary fibrosis?

A

Old age
Smoking
Male

216
Q

What happens in idiopathic pulmonary fibrosis?

A

Due to an unknown tigger, type II pneumocytes over proliferate, leading to excess myofibroblasts and therefore excess collagen deposition. The myofibroblasts also do not undergo normal apoptosis and therefore continue to make collagen.

217
Q

What is the consequence of the thickening/ fibrosis of the interstitial layer in pulmonary fibrosis?

A
  • The lungs get stiff, making it harder for air to get in and out
  • There is alveolar loss, with cysts replacing them
  • Problems with ventilation and oxygenation
218
Q

What are the key presentations of idiopathic pulmonary fibrosis?

A 
Coughing
SOB
Cyanosis
Clubbing
Symptoms worsen over time
219
Q

How is IPF diagnosed?

A

HRCT
Pulmonary function test
CXR
ABG

220
Q

What would be seen on a HRCT/ CXR in IPF?

A

Honeycomb appearance (due to cysts), thickening of interstitial walls.

221
Q

How is IPF managed?

A

Supplemental oxygen
Antifibrotic medications
Lung transplant

222
Q

What is the prognosis of IPF?

A

Poor- Life expectancy 2-5 years from diagnosis.

223
Q

What is hypersensitivity pneumonitis?

A

Restrictive interstitial lung disease caused by a type III hypersensitivity reaction.

224
Q

What are the most common triggers of the type III hypersensitivity reaction in hypersensitivity pneumonitits?

A 
Bird droppings
Mould
Dust
Hay
Mushrooms
225
Q

How does type III hypersensitivity affect the lungs?

A

On every exposure to the allergen, the immune system releases cytokines and inflammatory mediators which damage the lungs, causing fibrosis.

226
Q

How can hypersensitivity pneumonitis be diagnosed?

A

Bronchiolar lavage–> Washing airways with fluid and analysing fluid to look for lymphocytes and mast cells.

227
Q

What are the key causes of occupational lung disorders?

A

Coal
Dust
Silica
Asbestos

228
Q

How do particles affect the lungs in occupational lung disorders?

A

Macrophages pick them up and release chemokines which trigger an immune response. Immune cels release further cytokines which damage the alveolar epithelium and fibroblasts try to repair the damage by depositing collagen, causing fibrosis.

229
Q

What is the definition of pulmonary hypertension?

A

Increased resistance and pressure of blood in the pulmonary arteries, giving a mean pulmonary artery pressure (mPAP) of >25mmHg

230
Q

What does pulmonary hypertension cause?

A

Back pressure into the right side of the lung and systemic venous system.

231
Q

What is the cause of Group 1 pulmonary hypertension?

A

Primary pulmonary hypertension (idiopathic)

Connective tissue disease (e.g SLE)

232
Q

What is the cause of Group 2 pulmonary hypertension?

A

Left sided heart failure ( usually due to MI or systemic hypertension) causing back pressure into the lungs

233
Q

What is the cause of Group 3 pulmonary hypertension?

A

Chronic lung disease (e.g. COPD)- Cause fibrosis of the lung leading to vasodilation and therefore increased pressure in the pulmonary vessels

234
Q

What is the cause of Group 4 pulmonary hypertension?

A

Pulmonary vascular disease (e.g. pulmonary embolism)

235
Q

What are the causes of group 5 pulmonary hypertension?

A

Miscellaneous: sarcoidosis, glycogen storage disease, haematological disorders

236
Q

What are the main symptoms/ signs of pulmonary hypertension?

A 
Shortness of breath
Syncope
Tachycardia
Rasied JVP
Hepatomegaly/ Splenomegaly (caused by back pressure into spleen/ liver) 
Peripheral oedema
237
Q

What would be seen on an ECG with pulmonary hypertension?

A

Right hearted heart strain:

  • Larger R waves on right sided chest leads showing right ventricular hypertrophy
  • Right axis deviation
  • Right bundle branch block
238
Q

What investigations could be done to look for pulmonary hypertension?

A

ECG
CXR: Dilated pulmonary arteries, right ventricular hypertrophy
Raised NT-proBNP blood test (shows RV failure)
Echo

239
Q

How can primary pulmonary hypertension be managed?

A

Vasodilators:

  • IV prostanoids (vasodilators/antiplatelet)
  • Endothelin receptor antagonists
  • Phosphodiesterase-5 inhibitors
240
Q

What is the prognosis for pulmonary hypertension?

A

30-40% 5 year survival

241
Q

How is pulmonary hypertension (not primary) managed?

A

Treat underlying cause

Supportive treatment for complications

242
Q

What is pulmonary embolism?

A

When a blood clot (thrombus) forms in the pulmonary arteries

243
Q

What is the most common cause of pulmonary embolism?

A

Deep vein thrombosis that develops in the leg and embolisms through the right side of the heart to the pulmonary arteries.

244
Q

What is VTE?

A

Venous thromboembolism: When a DVT travels and causes PE

245
Q

What are the risk factors for developing a pulmonary embolism?

A 
Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy (oestrogen) 
Malignancy
SLE
Polycythaemia
Thrombophilia
246
Q

How is VTE avoided?

A

Those at risk recieve prohpylactic low molecular weight heparin
Embolic compression stockings.

247
Q

What are the contraindications of giving low MWH to a patient at risk of VTE?

A 
Active bleeding
Existing anticoagulation (e.g. Warfarin/ NOAC)
248
Q

What are the presentations of a pulmonary embolism?

A 
(can be subtle) 
Shortness of breath
Cough (with/ without blood) 
Pleuritic chest pain
Hypoxia
Tachycardia
Raised respiratory rate
Low grade fever
Haemodynamic instability (causes hypotension)
May be signs of DVT
249
Q

What is the Wells score?

A

The risk prediction of a patient having DVT or pulmonary embolism taking in to account their risk factors and clinical findings.

250
Q

How is pulmonary embolism diagnosed?

A

History
Examination
CXR
Wells score; if likely perform CT pulmonary angiogram

251
Q

What are the two ways of establishing a definitive diagnosis for pulmonary embolism?

A

CT pulmonary angiogram

V/Q (ventilation perfusion) scan

252
Q

What is a CTPA?

A

CT Pulmonary angiogram - involves chest CT scan with IV contrast that hilights the pulmonary arteries.

253
Q

What does a V/Q scan involve?

A

Radioactive isotopes inhales to fill the lungs and a picture taken to demonstrate ventilation.
Contrast containing isotopes injected and picture taken to demonstrate perfusion.
Pictures then compared.

254
Q

What happens to the V/Q with a pulmonary embolism?

A

Deficit in perfusion as the thrombus blocks blood flow to the lung tissue.

255
Q

What is usually seen in an ABG with pulmonary embolism?

A

Respiratory alkalosis. High resp rate causes them to blow off excess CO2, as well as low pO2

256
Q

How is a pulmonary embolism managed?

A

Oxygen and analgesia as required
Immediate anticoagulation (Low molecular weight heparin)
Long term anticoagulation (warfarin, NOAC, LMWH)
Thrombolysis

257
Q

When is thrombolysis used for a PE and how does it work?

A

When there is a massive PE with haemodynamic compromise.

Involves injecting fibrinolytic medication that rapidly dissolves clos.

258
Q

What is a pleural effusion?

A

Collection of fluid in the pleural cavity.

259
Q

What does exudative mean?

A

Fluid buildup caused by inflammation.

260
Q

What does transudative mean?

A

Fluid build up caused by systemic conditions that alter the blood pressure.

261
Q

What are the two main causes of pleural effusion?

A

Exudative and Transudative

262
Q

What happens in exudative pleural effusion?

A

Inflammation of the pulmonary capillaries causes fluid, proteins and immune cells to leak out of the tissues into the pleural space.

263
Q

What are the main causes of exudative pleural effusion?

A

Things that cause inflammation:

  • Trauma
  • Malignancy (lung cancer)
  • Inflammatory conditions (Lupus)
  • Infection (Pneumonia
    e. t.c.
264
Q

What happens in transudative pleural effusion?

A

Increased pressure in the vessels (hydrostatic pressure) or low blood protein count (low oncotic pressure) causes fluid to move into the pleural space.

265
Q

What are the main causes of transudative pleural effusion?

A
  • (Congestive) heart failure
  • -Liver cirrhosis (liver makes too few proteins)
  • Nephrotic syndrome (protein is lost in the urine)
  • Hypothyroidism
  • Melg’s syndrome
266
Q

How does pleural effusion present?

A

Pleurisy (Pain when inhaling)

Shortness of breath (Worse when lying down)

267
Q

What is the difference between pulmonary oedema and pleural effusion?

A

Pulmonary oedema happens when fluid collects in the lungs (alveoli).
Plueral effusion is when there is an accumulation of fluid in the pleural cavity

268
Q

What is the pleura comprised of?

A

Visceral pleura
Pleural cavity containing fluid
Parietal pleura

269
Q

What does the interstitial fluid contain and where does it come from?

A

Proteins such as albumin.

Leakage of fluid from the capillaries

270
Q

How does fluid drain from the pleural cavity?

A

Lymphatic drainage.

271
Q

What can happen if infection is the cause of exudative pleural effusion?

A

The infection can spread to the pleural space, like an abscess. The infected pleural space can develop fibrinous walls and loculation (enlarged fluid mass)

272
Q

What is chylotorax?

A

A lymphatic pleural effusion that occurs when there is a blockage in the thoracic duct, causing lymphatic fluid to accumulate in the pleural space.

273
Q

How is pleural effusion diagnosed?

A

Decreased breath sounds
Dullness to percussion
Decreased tactile fremitus (vibrations)
CXR

274
Q

What can be seen on a CXR in pleural effusion?

A 
Tracheal deviation is massive
Fluid (blunting) in the costophrenic angle if stood
Layered fluid if lying
Fluid in lung fissures
Larger effusions will have a meniscus.
275
Q

How is pulmonary effusion treated?

A

Thoracentesis to drain fluid and find out cause.

276
Q

What happens in a thoracentesis?

A

Hollow needle is inserted above a rib (to avoid neurovascular bundle) and fluid is drained.

277
Q

What does transudative fluid look like when drained?

A

Clear

278
Q

What does exudative fluid look like when drained?

A

Cloudy- full of immune cells

279
Q

What does lymphatic fluid look like when drained?

A

Milky- filled with fats

280
Q

How can you differentiate between transudative and exudative fluid?

A

Exudative: >3g protein/dL
Transudative: < 3g/dL

281
Q

How can small pleural effusions be treated?

A

Treat underlying cause:

Usually caused by heart failure: so diuretics and sodium restriction

282
Q

How can large effusions be treated?

A

Usually caused by cancer: Drainage with tube

283
Q

What are the usual causes of large loculated effusions and how are they treated?

A

Usually caused by pneumonia or tuberculosis. Treat with surgery as the fluid can form a paste (empyema)

284
Q

What is the fluid sample analysed for?

A 
Protein count
Cell count
pH
Glucose
LDH
Microbes
285
Q

What is empyema?

A

An infected pleural effusion

286
Q

What is pulmonary oedema?

A

Buildup of fluid in the interstitial space of the lungs

287
Q

What are the causes of pulmonary oedema?

A

Cardiogenic–> Left sided heart failure, sever systemic hypertension
Non-cardiogenic–> Pulonary infection, toxin inhalation, trauma, sepsis
Low oncotic pressure–> Malnutrition, liver failure, nephrotic syndrome

288
Q

What is a pneumothorax?

A

When the seal of the pleural space is punctured, allowing air to enter and the lungs to collapse.

289
Q

How is the pressure in the pleura usually maintained?

A

Two opposing forces:
1. Muscle tension of diaphragm and chest wall causing it to expand outwards
2. Elastic recoil of the lungs trying to pull it inwards.
This creates a vacuum.

290
Q

What is the pressure in the pleural space under normal circumstances and when there is pneumothorax?

A 
Normally= -5cm of water
Pneumothorax= 0cm of water
291
Q

What are the different types of pneumothorax?

A

Spontaneous (primary and secondary) pneumothorax
Traumatic pneumothorax
Tension pneumothorax

292
Q

What happens in a spontaneous pneumothorax?

A

Bullae (air pocket) forms on the surface of the lungs and breaks, forming a hole in the visceral pleura and allowing air to enter the pleural space

293
Q

When do bullae form?

A

When alveoli develop a tiny leak, allowing air to leak into the surrounding air tissue.

294
Q

What is a primary spontaneous pneumothorax?

A

When there is the absence of an underlying condition

295
Q

What is the usual presenting patient in a primary spontaneous pneumothroax?

A

Thin, tall adolescent male holding his breath.

296
Q

What is a secondary spontaneous pneumathorax?

A

One which develops due to an underlying condition such as Marfan’s, cystic fibrosis, emphysema or lung cancer

297
Q

What is traumatic pneumothorax?

A

When trauma causes a rip in the parietal pleura, allowing air to enter from outside into the pleural space.

298
Q

What is tension pneumothroax?

A

Can develop similarly to the others, but creates a one way valve allowing air to enter but not leave due to a flap of tissue.

299
Q

What are the complications of tension pneumothorax?

A

Over time, it causes pressure build up which can compress the heart and lungs and shift structures like the trachea. This can reduce the cardiac output.

300
Q

What are the main symptoms of pneumothorax?

A

Shortness of breath

Chest pain

301
Q

What are the main signs of pneumothorax?

A

Ascultations–> reduced breath sounds

Percussion–> Hyperresonant

302
Q

How is pneumothorax diagnosed?

A

Collapsed lung on X ray

Tension pneumothroax may show tracheal deviation

303
Q

How is pneumothorax treated?

A

Small—> Will clear up on its own

Large/ tension–> Insert chest tube to remove air.

304
Q

What are the main causes of pneumothorax?

A

Spontaneous
Trauma
Latrogenic (lung biopsy, mechanical ventilation or central line insertion)
Lung pathology (infection, asthma, COPD)

305
Q

How is a tension pneumothorax treated?

A

Insert a large bore cannula into the second intercostal space in the midclavicular line

306
Q

Where are chest drains inserted?

A

Triangle of safety, between:

  • 5th intercostal space (nipple line)
  • Mid axillary line
  • Anterior axillary line
307
Q

How common is lung cancer?

A

Third most common cancer

308
Q

What is the primary cause of lung cancer?

A

Cigarette smoking (80% cases)

309
Q

What are the main types of lung cancer?

A

Non small cell:

  • Adenocarcinoma (40%)
  • Squamous cell carcinoma (30%)
  • Large-cell carcinoma (10%)

Small cell lung cancer (15%)

310
Q

What is significant about small cell lung cancer?

A

It contains neurosecretory granules that can release neuroendocrine hormones, making it responsible for multiple paraneoplastic syndromes

311
Q

What are the main signs and symptoms of lung cancer?

A 
Shortness of breath
Cough
Haemoptysis
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy
312
Q

What investigations can be done to look for lung cancer?

A 
CXR
Staging CT scan
PET-CT 
Bronchoscopy with endobronchial ultrasound
Biopsy
313
Q

What we be seen in a lung cancer X-ray?

A

Hilar enlargement
Peripheral opacity (lesion in lung field)
Pleural effusion
Collapse

314
Q

What is the first line treatment of non-small cell lung cancer?

A

Surgery (Lobectomy–> Removing lung lobe containing tumour, or segmentectomy/ wedge resection)

315
Q

What other treatments are used for non-small cell lung cancer?

A

Radiotherapy can be curative

Chemotherapy to improve outcomes

316
Q

How is small cell lung cancer treated?

A

Chemotherapy and radiotherapy

317
Q

What type of lung cancer has a worse prognosis?

A

Small cell lung cancer

318
Q

What are the main extrapulmonary manifestations of lung cancer?

A

Recurrent laryngeal nerve palsy
Phrenic nerve palsy
Superior vena cava obstruction

319
Q

What is recurrent laryngeal palsy and how does it present?

A

When the recurrent laryngeal nerve is paralysed due to the cancer pressing on tit as it passes through the mediastinum. Presents with hoarse voice.

320
Q

What is phrenic nerve palsy and how does it present?

A

Phrenic nerve paralysis due to nerve compression, causing diaphragm weakness and therefore presenting as shortness of breath.

321
Q

Why is superior vena cava obstruction a complication of lung cancer and how does it present?

A

Caused by direct compression of the tumour on the superior vena cava. Presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest.

322
Q

What is Pemberton’s sign?

A

Medical emergency where raising the hands over the head causes facial congestion and cyanosis (caused by superior vena cava obstruction)

323
Q

What is Horner’s syndrome?

A

Triad of partial ptosis (upper eyelid drooping) , anhidrosis (absence of sweating of the face) and miosis (constriction of the pupil).

324
Q

What causes Horner’s syndrome?

A

Pancoast’s tumour (on the pulmonary apex) pressing on the sympathetic ganglion

325
Q

What is SIADH and how does lung cancer causes?

A

Syndrome of inappropriate ADH secretion caused by ectopic ADH secretion by a small cell lung cancer.

326
Q

How does SIADH present?

A

Hyponatraemia

327
Q

How can Cushing’s syndrome be caused by lung cancer?

A

Ectopic ACTH secretion by small cell lung cancer

328
Q

How can lung cancer cause hypercalcaemia?

A

Ectopic PTH secretion from a squamous cell carcinoma

329
Q

What is limbic encephalitis and how is it caused by lung cancer?

A

Where small cell lung cancer causes the immune system to make antibodies to tissues in the limbic system, causing inflammation.

330
Q

What are the symptoms of limbic encephalitis?

A

Short term memory impairment
Hallucinations
Confusion
Seizures

331
Q

What is Lamert-Eaton Myasthenic syndrome?

A

The symptoms caused by antibodies produced against small cell lung cancer targeting voltage-gated calcium channels on the presynaptic terminals in motor neurones

332
Q

What are the symptoms of Lamert-Eaton Myasthenic syndrome?

A 
Weakness- especially in proximal muscles and intraocular muscles (causing double vision -diplopia), Levetator muscles (causing ptosis- drooping) and pharyngeal muscles (causing slurred speech and dysphagia).
Autonomic dysfunction (dry mouth, blurred vision, impotence, dizziness)
333
Q

What is post-tetanic potentation and what is it a sign of?

A

Lambert-Eaton Myasthenic syndrome:

When their reduced tendon reflexes go back to normal for a short period after strong muscle contraction.

334
Q

What is mesothelioma?

A

A lung malignancy affecting the mesothelial cells of the pleura.

335
Q

What is the main risk factor in mesotheliuma?

A

Previous asbestos exposure.

336
Q

What is Goodpasture’s syndrome?

A

Rare autoimmune disease where anti-GBM antibodies attack the basement membrane of the lungs and kidneys, causing glomerulonephritis and pulmonary haemorrhage

337
Q

What is Wegener’s granulomatosis?

A

Rare form of vasculitis associated with ANCA antibodies.

338
Q

What is Whooping cough?

A

An upper respiratory tract infection that causes such severe coughing fits that the child is unable to take in any air between coughs and therefore makes a loud whooping sound as they forcefully suck in air after they finish coughing.

339
Q

What causes Whooping cough?

A

Bordetella pertussis (gram negative bacteria)

340
Q

Who is vaccinated against pertussis (whooping cough bactera)?

A

Children and pregnant women

341
Q

What are the initial symptoms of Whooping cough?

A

Mild coryzal symptoms (inflammation of mucous membrane in nasal cavity–> head cold)
Low grade fever
Mild dry cough

342
Q

How do the symptoms of whooping cough progress?

A

More severe coughing fits after a week or more (paroxysmal: sudden attacks)
May cough so hard they faint, vomit or even get pneumothorax

343
Q

How is whooping cough diagnosed?

A

Nasopharyngeal/ nasal swab with PCR testing or bacterial culture.
If present for >2 weeks, can test for anti-pertussis toxin immunoglobulin G

344
Q

How is Pertussis managed?

A
  • Notify public health
  • Supportive care
  • Measures to prevent spread
  • Macrolide antibiotcs can be beneficial in the first 21 days or in vulnerable patients
345
Q

How long does whooping cough generally last?

A

6-10 weeks

346
Q

What is given to people who have had close contact with an infected patient?

A

Prophylactic antibiotics

347
Q

What is a key complication of whooping cough?

A

Bronchiectasis

348
Q

What is Croup?

A

An acute upper respiratory tract infection affecting young children.

349
Q

What age group does Croup usually affect?

A

children aged 6 months to 2 years

350
Q

What are the most common causes of croup?

A

Parainfluenza virus
Influenza
Adenovirus
Respiratory syncytial virus

351
Q

What are the key presentations of Coup?

A 
Larynx oedema causing: 
Increased work of breathing
'Barking' cough episodes
Hoarse voice
Stridor (high pitched breathing) 
Low grade fever
352
Q

How is Croup managed?

A 
Simple supportive treatment (fluids & rest) 
Oral dexamethasone (very effective) - single dose usually given which can be repeated
353
Q

How long does Croup ususally last?

A

48 hours.

354
Q

Where does the upper respiratory tract end?

A

Nose–> Larynx (above the vocal cords)

355
Q

What is pneumonia?

A

Infection of the lung tissue

356
Q

What is consolidation on an X-ray?

A

When the air in the lungs is replaced by something else (e.g. blood, pus, water or solid), showing a white area

357
Q

What does pneumonia do to the lung tissue?

A

Causes inflammation of the lung tissue and results in sputum filling the airways and alveoli.

358
Q

What is community acquired pneumonia and what is the other type?

A

Pneumonia that develops outside of hospital.

If it develops >48 hours after hospital admission, it is ‘hospital acquired pneumonia)

359
Q

What is aspiration pneumonia?

A

Pneumonia that develops as a result of aspiration–> Inhaling foreign material such as food.

360
Q

How does pneumonia typically present?

A 
Shortness of breath
Cough productive of sputum
Fever
Haemoptysis
Pleuritic chest pain
Delirium
Sepsis
361
Q

What are the signs of pneumonia?

A 
Tachypnoea (raised respiratory rate) 
Tachycardia
Hypoxia (low oxygen) 
Hypotension (shock) 
Fever
Confusion
362
Q

What are the characteristic chest sounds in pneumonia?

A

Bronchial breath sounds (harsh sound equally loud on inspiration and expiration)
Focal course crackles (air passing through sputum in the airways )
Dullness to percussion (due to lung tissue collapse/ consolidation)

363
Q

What scoring system is used to asses the severity of pneumonia?

A 
CURB-65 in hospital.
 C: confusion
U: urea >7
R: respiratory rate >30 
B: blood pressure< 90 systolic/ <60 diastolic 
65: Age> 65

(CRB-65 out of hospitals as can’t test urea)

364
Q

What CRB-65 score would indicate the need to refer to hospital?

A

Anything other than 0-1.

If >3, take to intensive care

365
Q

What are the common causes of pneumonia?

A

Strep. pneumoniae

Haemophilus influenzae

366
Q

What are other causes of penumonia and their associations?

A 
Moraxella catarrhalis (in immunocompromised patients with chronic pulmonary disease)
Pseudomonas aerginosa (in patients with cystic fibrosis or bronchiectasis)
Staph. aureus (in patients with cystic fibrosis)
367
Q

What is atypical pneumonia?

A

Pneumonia that is caused by an organism that cannot be cultured in the normal way or detected using a gram stain.

368
Q

How can atypical pneumonias be treated?

A

(don’t respond to penicillin)
Macrolides
Fluroquinolones
Tetracyclines

369
Q

What are the 5 causes of atypical pneumonia?

A 
Legionella pneumophila (Legionnaires' disease) 
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Coxiella burnetii
Chlamydia psittaci
370
Q

What is Legionnaires’ disease and what are the typical causes/ presentations?

A

Type of atypical pneumonia caused by infected air supplies or air conditioning units (e.g. someone on a cheap holiday).
Presents with hyponatramia due to SIADH

371
Q

What is mycoplasma pneumoniae and what are the typical symptoms?

A

Milder cause of pneumonia that can cause a rash (erythema multiforme), characterised by varying sized target lesions.
Can also cause neurological symptoms.

372
Q

What is Chlamydophila pneumoniae?

A

Mild/ moderate atypical pneumonia presenting with a wheeze (usually school aged child)

373
Q

What is Coxiella burnetii and what is the usually cause + presenting patient?

A

Atypical pneumonia linked to exposure to animals and their bodily fluids (usually a farmer with a flu like illness)

374
Q

What is chlamydia psittaci and how is it caused/ presenting patient?

A

Contact with infected birds (e.g. parrot owner)

375
Q

What is pnuemocystis jiroveci and when does it occur?

A

Type of funfal pneumonia that occurs in patients who are immunocompromised.

376
Q

Which patients are most at risk of fungal pneumonia?

A

Patients with poorly controlled/ new HIV with low CD4 count.

377
Q

How does fungal pneumonia present?

A

Dry cough without sputum
Shortness of breath on exertion
Night sweats

378
Q

How is fungal pneumonia treated?

A

Co-trimoxazole (Septrin)

379
Q

How is pneumonia investigated?

A 
CRB-65 assessment
Chest X ray
FBC (Raised WCC)
U&E's (for urea)
CRP (Raised in inflammation/ infection)
380
Q

What investigations should be done in moderate-severe pneumonia cases?

A

Sputum cultures
Blood cultures
Legionella and pneumococcal urinary antigens

381
Q

How can pneumonia progression be monitored?

A

Inflammatory markers (WCC/CRP) are raised in proportion to the severity of the infection, so can monitor this to see the progress.

382
Q

Which out of WCC and CRP gives a more accurate indication of how well antibiotics are working?

A

WCC- Responds faster than CRP

383
Q

How is pneumonia generally treated?

A

Antibiotics:
Mild CAP: 5 day course of oral antibiotics (amoxicillin/ macrolide)
Moderate-severe CAP: 7-10 day course of dual antibiotics

384
Q

What are the main complications of pneumoia?

A 
Sepsis
Pleural effusion
Empyema
Lung abscess
Death
385
Q

What is TB?

A

Tuberculosis is an infectious disease caused by the mycobacterium tuberculosis.

386
Q

What causes TB?

A

Mycobacterium tuberculosis bacteria

387
Q

What kind of bacteria is TB?

A

Acid-fast bacilli (small rod shaped bacteria that is resistant to the acids in gram staining)

388
Q

What staining is necessary to see the presence of TB?

A

Zeihl-Neelsen stain

389
Q

What would be seen on a stain of TB?

A

Bright red bacilli against a blue background

390
Q

Where is TB more prevelant?

A

Africa and South Asia

391
Q

What are MDR TB?

A

Multi-drug resistant TB, strains that are resistant to more than one TB drug making them difficult to treat

392
Q

How is TB spread?

A

Inhaling saliva droplets from infected people

393
Q

Why is TB very difficult to culture and treat?

A

It is very slow dividing with high oxygen demands

394
Q

How does TB spread in the body?

A

Through the lymphatics and blood, granulomas containing it form throughout the body

395
Q

What is active TB?

A

When there is active infection in various areas of the body.

396
Q

What is latent TB?

A

When the immune system encapsulates sites of infection to stop the progression of the disease.

397
Q

What is secondary TB?

A

When latent TB reactivates

398
Q

What is miliary TB?

A

When the immune system is unable to control the disease, causing a disseminated severe disease

399
Q

Where is the most common site for TB infection and why?

A

The lungs, where they get plenty of oxygen

400
Q

Where are the main sites of extrapulmonary TB?

A 
Lymph nodes
Pleura
CNS
Pericardium
GI/ GU system
Bones/ joints
Cutaneous (skin)
401
Q

What are the risk factors for TB?

A

Known contact with active TB
Immigrants from areas of high TB prevalence
Relatives/ close contacts from countries with high TB rate
Immunosuppression
Homeless people, drug users, alcoholics

402
Q

What vaccine can be used to protect against severe/ complicated TB?

A

BCG vaccine

403
Q

What does the BCG vaccine involve?

A

Intradermal infection of live attenuated (weakened) TB

404
Q

What test are patients given prior to TB vaccine and why?

A

Mantoux test to test for TB

405
Q

Who is the BCG vaccine offered to?

A

Neonates:
-In areas of the UK with high rates of TB
-With relatives from countries with high TB rates
- With family history of TB
Unvaccinated people <35 who have close contact with TB or have just arrived from a country with high TB rate
Healthcare workers

406
Q

How does TB usually present?

A

With history of chronic, gradually worsening symptoms

407
Q

What are the signs/ symptoms of TB?

A 
Lethargy
Fever/ night sweats
Weight loss
Cough (may be haemoptysis)
Lymphadenopathy
Erythema nodosum
Spinal pain
408
Q

What is erythema nodosum?

A

Inflammation of subcutaneous fat, presenting as tender red nodes on the anterior shins

409
Q

What percentage of TB cases are pulmonary TB?

A

70%

410
Q

How can TB be diagnosed?

A

(Very difficult)

  • Ziehl-Neelsen stain
  • Tests for immune response to TB caused by previous, latent or active TB: Mantoux test, Interferon-gamma release assay
  • CXR + Cultures to support diagnosis
411
Q

What is the Mantoux test?

A

Used to look for previous immune response to TB.

Tuberculin is injected into the intradermal space on the forearm, a bleb forms and after 72 hours is measured?

412
Q

What is tuberculin?

A

Collection of tuberculosis proteins that have been isolated from the bacteria, used to test for previous immune response to TB

413
Q

What Mantoux test results indicates previous TB infection?

A

Induration of >5mm

414
Q

What are interferon-gamma release assays?

A

Test for previous TB infection.

Sample of blood is taken and mixed with antigens from the TB bacteria.

415
Q

What happens in an interferon-gamma release assay if a person has had previous exposure to TB?

A

White blood cells are sensitised to TB antigens, so release inteferon-gamma as part of the immune response.

416
Q

When is the IGRA test used?

A

In patients that do not have features of active TB but do have a positive Mantoux test to confirm a diagnosis of latent TB

417
Q

What would be seen in a CXR of primary TB?

A
  • Patchy consolidation
  • Pleural effusions
  • Hilar lymphadenopathy
418
Q

What would be seen in a CXR of reactivated TB?

A

Patchy/ nodular consolidation with cavitation (gas filled spaces in the lungs)

419
Q

What would be seen in a CXR of disseminated miliary TB?

A

‘Millet seeds’ uniformly distributed throughout lung fields

420
Q

What needs to be done before beginning treatment of TB and why?

A

Bacterial culture, to allow testing for antibiotic resistance

421
Q

What are the different methods of taking bacterial cultures?

A

Sputum
Mycobacterium blood cultures
Lymph node aspiration/ biopsy

422
Q

What test can be done to look for the DNA of TB bacteria and why/ when is it used?

A

Nucleic acid amplification test
Provides information about the bacteria faster than a traditional culture (only used when this information would affect treatment or they are at higher risk of developing complications)

423
Q

How is latent TB managed?

A

Healthy patients do not need treatment.
Patients at risk of reactivation can be treated with:
-Isoniazid/ Rifampicin for 3 months
-Isoniazid for 6 months

424
Q

How is acute TB managed?

A 
RIPE:
Rifampicin (6 months)
Isoniazid (6 months)
Pyrazinamide (2 months)
Ethambutol (2 months)
425
Q

What is a side effect of isoniazid and what is often prescribed along side to prevent it?

A

Isoniazid causes peripheral neuropathy so pyridoxine (vit B6) is usually co-prescribed prophylactically to help prevent it.

426
Q

Other than medications, what other management options need to be considered for TB treatmemt?

A

Test for other infectious diseases
Test contacts for TB
Notify Pulbic health
Isolate patients/ use negative pressure rooms to prevent spread until they are on established treatment.
Steroids used if disease is extrapulmonary
Individualised drug regime needed for MDR TB

427
Q

What are the side effects of TB treatment?

A

Rifampicin: can cause red/ orange discolourations of secretions and reduces effect of metabolised drugs (e.g. the pill)
Isoniazid: Can cause peripheral neuropathy
Pyrazinamide: Can cause hyperuricaemia leading to gout
Ethambutol: Can cause colour blindness
All associated with hepatotoxicity

PHASE 2A (Mine) (15 decks)

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