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Phase 2A Tom > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is COPD?

A

Describes progressive and irreversible obstructive airway disease. It is a combination of emphysema and chronic bronchitis

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2
Q

Describe the epidemiology of COPD

A
  • 1.2 million people in the UK
  • 4th leading cause of death globally
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3
Q

What are the risk factors for developing COPD?

A
  • Tobacco smoking (biggest risk factor)
  • Air pollution
  • A1AD
  • Occupational exposure such as dust, coal, cotton, cement and grain
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4
Q

What are the two things that make up COPD?

A

Emphysema and bronchitis

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5
Q

What is emphysema?

A

Alveolar air sacs become damaged or destroyed:
- They become enlarged and lose their elasticity.
- Individuals have difficulty exhaling which depends heavily on lung recoil

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6
Q

Describe the pathophysiology of emphysema

A
  • When lung tissue is exposed to irritants it triggers an immune response
  • This attracts various immune cells such as elastases and collagenases which causes a loss in elastin in the alveoli

The elastin loss causes collapse meaning:
- air is trapped distal to the point of collapse
-lungs become more compliant when air is inhaled, the lungs expand easily and hold onto air
- Breakdown if the thin alveolar walls, which reduces the surface area for gas exchange

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7
Q

What are some signs of emphysema?

A
  • Barrel shaped chest due to air trapping and hyperinflation
  • Downward displacement of liver due to hyperexpansion of the lungs
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8
Q

What is bronchitis?

A

Inflammation of the bronchial tubes of the lungs. It is said to be chronic when it causes a productive cough for at least 3 months every year for 2 or more years

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9
Q

Describe the pathophysiology of chronic bronchitis?

A

-Due to chemicals and irritants the squamous epithelium may become ulcerated and when it heals it is replaced with columnar cells (metaplasia). Irritants also stimulate hypertrophy and hyperplasia of mucinous glands so there is an increase in mucus production in bronchioles with narrow lumen this can cause obstruction

  • This inflammation is also followed by scarring and thickening of the walls which narrows the small airways and makes cilia shorter making it harder to move mucus meaning coughing is the only way to remove it

Overall, there is airway narrowing due to hyperplasia, inflammation and oedema.

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10
Q

Why is there V/Q mismatch in COPD?

A

Due to damage and mucus plugging of smaller airways. This leads to a fall in PaO2 and increased respiration. CO2 will remain unaffected until patient can no longer maintain respiratory effort

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11
Q

What is the usual drive for respiration and how does this change in how does this change in COPD?

A

The usual drive for respiration is CO2 however body becomes desensitised to high CO2.
- Hypoxaemia becomes the new drive for respiration.

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12
Q

What are the signs of COPD?

A
  • Tachypnoea
  • Barrel chest
  • Cyanosis
  • Quiet breath sounds and wheeze
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13
Q

What are the symptoms of COPD

A
  • Dyspnoea
  • Productive cough
  • Wheeze
  • Chest tightness
  • Weight loss
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14
Q

What are signs of CO2 retention?

A
  • Drowsy
  • Asterixis (flapping tremor of hands)
  • Confusion
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15
Q

What are the differentials for COPD?

A
  • Lung cancer, lung fibrosis or heart failure
  • COPD does not cause clubbing or haemoptysis/chest pain
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16
Q

What is the MRC dyspnoea scale?

A

5 point scale for assessing impact of breathlessness.

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 their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness

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17
Q

What would happen to FVC (max air exhaled in one breath) in COPD?

A

It would be lowered

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18
Q

What would happen to FEV1 (first second of air breathed out in a single breath) in COPD?

A

Lowered more than FVC

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19
Q

What would happen to TLC in COPD?

A

Increased due to air trapping

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20
Q

How would you make a diagnosis of COPD?

A
  • Clinical presentation plus spirometry
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21
Q

What would spirometry show for COPD?

A

FEV1/FVC ratio less than 0.7

Important to note that it does not show a dramatic response to reversibility testing with salbutamol (beta-2 agonist). If it does then consider asthma as a differential

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22
Q

What is used to classify the severity of airway obstruction?

A

GOLD classification
Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted

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23
Q

What other investigations might you perform for COPD?

A
  • Chest x-ray to rule out other pathology
  • BMI for a baseline to asses weight loss/weight gain form steroids
  • ECG
  • CT thorax to rule out fibrosis, cancer or bronchiectasis
  • Serum alpha-1 antitrypsin
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24
Q

What is the initial management for COPD?

A

STOP SMOKING

  • Annual flu vaccine and the pneumococcal vaccine (this is a one off vaccine)
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25
Q

What are the GOLD groups in COPD?

A

GOLD A= 1 or less exacerbations per year not requiring admission with mild symptoms
GOLD B= 1 or less exacerbations per year not requiring admission with severe symptoms
GOLD C= 2 exacerbations per year or 1 per year requiring admission with mild symptoms
GOLD D= 2 exacerbations per year or 1 per year requiring admission with severe symptoms

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26
Q

What are the different bronchodilators used to treat COPD?

A
  • SABA:short-acting beta-agonist (e.g. salbutamol)
  • SAMA: short-acting muscarinic antagonist (ipratropium)
  • LABA: long-acting beta-agonist (e.g. salmeterol)
  • LAMA: long-acting muscarinic antagonist (e.g. tiotropium)
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27
Q

What is the treatment for GOLD group A?

A

Any short or long acting bronchodilator

(saba/laba)

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28
Q

What is the treatment for GOLD group B?

A

LAMA/LABA

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29
Q

What is the treatment for GOLD group C?

A

LAMA

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30
Q

What is the treatment for GOLD group D?

A

LAMA or LABA+LAMA or LABA+ICS (ICS: inhaled corticosteroid (e.g. beclomethasone)

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31
Q

When is long term oxygen therapy used to treat COPD?

A

Long term oxygen therapy is used for severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale). It can’t be used if they smoke as oxygen plus cigarettes is a significant fire hazard.

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32
Q

What is an exacerbation of COPD?

A

COPD presents as an acute worsening of symptoms such as cough, shortness of breath, sputum production and wheeze

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33
Q

What causes an exacerbation of COPD?

A
  • Usually triggered by viral or bacterial infection
  • Can be heart failure, pulmonary embolism or medications
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34
Q

What would an exacerbation of COPD look like on an ABG?

A
  • CO2 will make blood more acidotic. This will show as a type 2 respiratory acidosis high CO2 and low oxygen with low pH
  • If this chronic there will be some metabolic compensation by kidneys releasing more bicarbonate to try and neutralise pH
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35
Q

What would an exacerbation look like on an ABG?

A
  • CO2 will make blood more acidotic. This will show as a type 2 respiratory acidosis high CO2 and low oxygen with low pH
  • If this chronic there will be some metabolic compensation by kidneys releasing more bicarbonate to try and neutralise pH
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36
Q

What is the treatment for an exacerbation of COPD where the patient is well enough to stay at home?

A
  • Prednisolone for 7-14 days
  • Regular inhalers or home nebulisers
  • Antibiotics if there is presence of infection
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37
Q

What is the treatment for an exacerbation of COPD where the patient is in hospital?

A
  • Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h)
  • Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone)
  • Antibiotics if evidence of infection
  • Physiotherapy can help clear sputum
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38
Q

What are the treatment options for an exacerbation of COPD not responding to treatment?

A
  • IV aminophylline
  • Non-invasive ventilation
  • Intubation and ventilation
  • Doxapram can be used as a respiratory stimulant if ventilation not appropriate
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39
Q

Why do you have to be careful giving oxygen to someone with COPD and how would you manage this?

A
  • Too much oxygen in someone that is prone to retaining CO2 can depress their respiratory drive.
  • Venturi masks are designed to deliver specific percentage concentrations of oxygen
  • If retaining CO2 aim for oxygen saturations of 88-92% titrated by Venturi mask
  • If not retaining CO2 and their bicarbonate is normal (meaning they do not normally retain CO2) then give oxygen to aim for oxygen saturations > 94%
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40
Q

What is asthma?

A
  • A chronic inflammatory airway disease characterised by intermittent airway obstruction and hyperreactivity
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41
Q

What are the two types of asthma?

A
  • Allergic/eosinophilic
  • Non-allergic e.g. exercise, cold air and stress
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42
Q

What are some risk factors for developing asthma?

A
  • History of atopy (allergies)
  • Viral URTI
  • Occupational exposure
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43
Q

What causes asthma?

A
  • There is often an excessive reaction for the Th2 cells against specific antigens. Allergens from environmental triggers are picked up by dendritic cells and presented to Th2 cells leading to the release of cytokines.
  • This leads to the production of IgE antibodies which lead to histamine release
  • dendritic cells -> TH2 -> cytokines -> IgE -> histamine
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44
Q

What are some genetic causes of asthma ?

A
  • Genes controlling cytokines IL-3 -4 -5 -9 -13
  • ADAM33 is associated with airway hyper-responsiveness and tissue remodelling

Generally asthma before 12 is more genetic after this it is more environmental

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45
Q

What is the hygiene hypothesis?

A

Reduced early immune-system exposure to bacteria and viruses might increase the risk of later developing asthma, possibly by altering the overall proportion of immune cell subtypes.

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46
Q

What are the signs and symptoms of asthma?

A
  • Episodic
  • Diurnal variability- worse at night and in the morning
  • Dry cough with wheeze and shortness of breath
  • Bilateral widespread “polyphonic” wheeze heard by a healthcare professional
  • Family history of other ectopic disease such as eczema and hayfever
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47
Q

What are the primary investigations for asthma?

A
  • Fractional exhaled nitric oxide a value of >40 ppb is positive
  • Spirometry will show a FVC/FEV1 ratio of less than 70% but will improve by 12% and increase by >200ml when using a bronchodilator
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48
Q

What tests would you perform if you were unsure of a diagnosis of asthma?

A
  • PEFR: measured multiple times a day over a 2-4 week period. Variability of >20% throughout the day is diagnostic
  • Airway hyperreactivity testing: a histamine or methacholine direct bronchial challenge
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49
Q

What are Short acting beta 2 adrenergic receptor agonists?

A

They work quickly but the effect only lasts for an hour or 2. Nor Adrenalin acts on smooth muscle of airways to cause relaxation.

Reliver or rescue medication salbutamol

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50
Q

What are Long-acting beta 2 agonists (LABA)?

A

Same as short acting but last for longer salmeterol

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51
Q

What are Long-acting muscarinic antagonists (LAMA)?

A

They block acetylcholine receptors =stimulated by the parasympathetic nervous system which cause bronchoconstriction.

tiotropium is an example

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52
Q

What are Inhaled corticosteroids (ICS)?

A

They reduce inflammation and reactivity of the airways. They are used for maintenance and prevention.

Beclomethasone

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53
Q

What are Leukotriene receptor antagonists?

A

Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion.

Montelukast

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54
Q

What is MART?

A

Maintenance and Reliever Therapy (MART). This is a combination inhaler containing a low dose inhaled corticosteroid and a fast acting LABA. This replaces all other inhalers and the patient uses this single inhaler both regularly as a “preventer” and also as a “reliever” when they have symptoms.

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55
Q

What is the BTS/SIGN stepwise ladder for treatment of asthma?

A
  1. SABA as required for wheezy episodes
  2. Regular low dose ICS inhaler
  3. Add LABA e.g. salmeterol
  4. Consider LTRA e.g. Montelukast or oral beta 2 agonist, oral theophylline or an inhaled LAMA (i.e. tiotropium).
  5. Titrate up ICS
  6. Add oral steroids at lowest possible dose
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56
Q

What is the NICE Guidelines (adapted from 2017 guidelines) for asthma

A
  1. SABA as required or wheezy episodes
  2. Regular lose dose ICS inhaler
  3. Add LTRA e.g. Montelukast
  4. Add LABA
  5. Consider MART
  6. Increase steroid dose
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57
Q

What are the triggers for an asthma attack?

A
  • Allergy exposure
  • Viral infection
  • Smoking exposure
  • Pollution
  • Exercise
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58
Q

What is the presentation of an asthma attack?

A
  • Fast respiratory rate
  • Symmetrical wheeze
  • Tight sounding chest with reduced air entry
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59
Q

What is investigated in an asthma attack?

A
  • PEFR
  • ABG: patients will initially have respiratory alkalosis. Abnormal or high PCO2 is concerning as it implies the patient is tiring
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60
Q

What would be considered an moderate asthma attack?

A
  • PEFR 50-75% of predicted
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61
Q

What would be considered a severe asthma attack?

A
  • PEFR 33-50%
  • Resp rate >25
  • Heart rate above 110
  • unable to complete sentences
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62
Q

What would be considered a life threatening asthma attack?

A
  • PEFR <33%
  • Sats <92%
  • Becoming tired
  • No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
  • Haemodynamic instability (i.e. shock)
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63
Q

What is the treatment for a moderate asthma attack?

A
  • Nebulised salbutamol
  • Nebulised ipratropium bromide
  • Steroids oral continue for 5 days after
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64
Q

What is the treatment for a severe asthma attack?

A
  • Oxygen is required to maintain stats
  • Aminophylline infusion
  • Consider IV salbutamol
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65
Q

What is the treatment for a life threatening asthma attack?

A
  • IV magnesium sulphate
  • Admission to ICU
  • Intubation in worst cases
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66
Q

What is TB?

A
  • Is an infectious disease caused mycobacterium tuberculosis
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67
Q

What type of bacteria is mycobacterium tuberculosis?

A
  • It is a small rod shaped bacteria. They are resistant to acids used in staining procedure so known as acid-fast bacilli.
  • Require a Zeihl-neelsen stain and is red
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68
Q

Describe the epidemiology of TB

A
  • 1.7 billion people worldwide have latent TB
  • Common in South Asia and sub-Saharan Africa
  • Prevalent in immunocompromised patients
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69
Q

How does TB cause disease?

A
  • Macrophages struggle to clear TB due to its waxy mycolic acid capsule.
  • A focal caseating granuloma typically forms in the lower lobe known as a Ghon focus. This creates a type IIII hypersensitivity reaction

-The TB bacteria are very slow dividing with high oxygen demands. It spreads via respiratory droplets from patients with active disease

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70
Q

What is latent TB?

A
  • Occurs after primary infection patients will remain asymptomatic and the bacteria remain dormant, resulting innegative sputumcultures but apositive Mantoux test.
  • The patient is not infectious but it can reactivate in immunocompromised individuals
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71
Q

What is secondary TB?

A
    • Reactivation typically occurs in thelung apexwhere pO2is highest, as mycobacteria are aerobic.
  • The bacteria can spread locally, to form caseating granulomata, or systemically (miliary TB).
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72
Q

What is miliary TB?

A
  • Occurs due to lympho-hematogenous spread to multiple organs e.g. heart, lungs, spleen, liver, bone marrow, pancreas and brain
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73
Q

What is the BCG vaccine?

A
  • Involves an intradermal infection of live attenuated TB. It offers protection against severe and complicated TB
  • Prior to vaccine patients are tested with Mantoux test
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74
Q

Who is offered the BCG vaccine?

A

BCG vaccine is offered to patients that are at higher risk of contact with TB:

  • Neonates born in areas of the UK with high rates of TB
  • Neonates with relatives from countries with a high rate of TB
  • Neonates with a family history of TB
  • Unvaccinated older children and young adults (< 35) who have close contact with TB
  • Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
  • Healthcare workers
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75
Q

What are the signs and symptoms of TB?

A
  • Lethargy
  • Fever or night sweats
  • Weight loss
  • Cough
  • Lymphadenopathy
  • Erythema nodosum
  • Spinal pain in spine TB also know as Pott’s disease of the spine
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76
Q

What is the Mantoux test?

A

This involves injecting tuberculin into the intradermal space on the forearm. Tuberculin is a collection of tuberculosis proteins that have been isolated from the bacteria. The infection does not contain any live bacteria.

Injecting the tuberculin creates a bleb under the skin. After 72 hours the test is “read”. This involves measuring the induration of the skin at the site of the injection.

NICE suggest considering an induration of 5mm or more a positive result. After a positive result they should be assessed for active disease.

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77
Q

What is the Interferon-Gamma Release Assays (IGRAs) test?

A

-The test involves taking a sample of blood and mixing it with antigen from the TB bacteria.

  • In a person who has had previous contact with TB there WBC will have become sensitised and they will release interferon gamma as part of an immune response
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78
Q

What are the tests performed in active TB?

A
  • CXR
  • Bacterial culture, collected from sputum, blood culture or lymph node aspiration
  • NAAT rapid diagnostic test done on sputum or urine
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79
Q

What would a CXR show for TB?

A
  • Primary TB may show patchy consolidation, pleural effusions and hilar lymphadenopathy
  • Reactivated TB may show patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones
  • Disseminated Miliary TB give a picture of “millet seeds” uniformly distributed throughout the lung fields
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80
Q

What is the management for latent TB?

A
  • Isoniazid and rifampicin for 3 months
  • Isoniazid for 6 months only

Isoniazid can often cause peripheral neuropathy. Pyridoxine (vitamin B6) is prescribed to prevent this

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81
Q

In what circumstances is it recommended to perform surgery in TB?

A

when tom makes duplicate flashcards

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82
Q

What is the management of acute pulmonary TB?

A

R- Rifampicin for 6 months
I- Isoniazid for 6 months
P- Pyrazinamide for 2 months
E- Ethambutol for 2 months

RIPE- all these drugs are associated with hepatotoxicity

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83
Q

What are the side effects of rifampicin?

A
  • Reduces the effect of drugs metabolised by cytochrome p450 e.g. contraceptive pill
  • Causes red/orange discoloration of secretions
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84
Q

What are the side effects of isoniazid?

A

Peripheral neuropathy

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85
Q

What are the side effects of pyrazinamide?

A

Can cause hyperuricaemia resulting in gout

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86
Q

What are the side effects of ethambutol?

A

Can cause colour blindness and reduced visual activity

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87
Q

What is the prognosis for TB?

A

5% mortality with treatment and 50% without

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88
Q

What is pneumonia?

A

A infection of the ling tissue and sputum filling the airways and alveoli. Can be seen as consolidation on a chest x-ray

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89
Q

What are the different types of pneumonia?

A
  • Community acquired
  • Hospital acquired if it occurs more than 48 hours after admission
  • Aspiration pneumonia if it occurs after inhaling foreign material
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90
Q

What are the main causes of CAP?

A
  • Streptococcus pneumonia (50%)
  • H. Influenzae (20%)
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91
Q

What are the main causes of HAP?

A

P.aeurginosa
E.coli
S.aureus
Klebsiella

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92
Q

What is the main cause of aspiration acquired pneumonia?

A

Klebsiella

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93
Q

What is the pathophysiology of pneumonia?

A
  • Pneumonia refers to any inflammatory reaction affecting the alveoli it is most commonly secondary to infection
  • The inflammation brings water into the lung tissue which makes it harder to breathe
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94
Q

What is atypical pneumonia?

A

It is a pneumonia caused by an organism that cannot be cultured in the normal way or detected on a gram stain.

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95
Q

What are the 5 causes of atypical pneumonia

A
  • Legionella pneumophila (Legionnaires’ disease). This is typically caused by infected water supplies or air conditioning units. It can cause hyponatraemia (low sodium) by causing an SIADH.
  • Mycoplasma pneumoniae- causes a rash called erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms in young patient in the exams.

Chlamydophila pneumoniae- school aged children with pneumonia

Q fever Coxiella burnetii, exposure to animals and their bodily fluids

Chlamydia psittaci. This is typically contracted from contact with infected birds. The MCQ patient is a from parrot owner.

Legions of psittaci MCQs

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96
Q

What are the signs and symptoms of pneumonia?

A
  • SOB
  • Cough productive of sputum
  • Fever
  • Haemoptysis
  • Pleuritic chest pain (worse on inspiration)

LOOK FOR SEPSIS

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97
Q

What is the presentation of atypical pneumonia?

A
  • Dry cough
  • Mild dyspnoea
  • Flu-like symptoms
  • Mild or no fever
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98
Q

What are the 3 characteristics chest signs of pneumonia?

A
  • Bronchial breath sounds: these are harsh breath sounds equally loud on inspiration and expiration
  • Focal coarse crackles- air pasing through the sputum causes sound
  • Dullness to percussion due to lung tissue collapse
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99
Q

What are the primary investigations for pneumonia?

A
  • CXR- will show consolidation (atypical pneumonia causes interstitial inflammation instead so may not show)
  • Chest x-ray
  • FBC (raised white cells)
  • CRP (raised in inflammation and infection)
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100
Q

What other investigations would be performed for more severe cases of pneumonia?

A
  • Sputum cultures
  • Blood cultures
  • Legionella and pneumococcal urinary antigens (send a urine sample for antigen testing)
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101
Q

What is used to test the severity of pneumonia?

A

C- Confusion
U- Urea >7
R- Respiratory rate >30
B- Blood pressure below 90/60
65- age over 65

If score of 1 then consider treatment at home
If score of 2 or more then consider hospital admission
If score of 3 or more than consider intensive care assessment

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102
Q

What is the treatment for CAP?

A
  • Low severity: oral amoxicillin or doxycycline/clarithromycin if penicillin allergy (5 days)
  • Moderate severity: amoxicillin and clarithromycin
  • High severity: IV co-amoxiclav and clarithromycin
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103
Q

What is the treatment for HAP?

A
  • Low severity: Oral co-amoxiclav
  • High severity: broad-spectrum e.g. IV tazocin or ceftriaxone add vancomycin if MRSA suspected
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104
Q

What is the prognosis for pneumonia?

A
  • CURB-65 of 0-1: low risk (<3% mortality)
  • CURB-65 of 2: intermediate risk (3-15% mortality)
  • CURB-65 of 3-5: high risk (>15% mortality)
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105
Q

What is pneumocystis pneumonia?

A

An opportunistic respiratory infection caused by the fungus, Pneumocystis jirovecii.

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106
Q

Who is at risk of pneumocystis pneumonia?

A

People with HIV/AIDS or who are immunosuppressed

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107
Q

What is the treatment for pneumocystis pneumonia?

A
  • Trimethoprim/sulfamethoxazole (co-trimoxazole):first-line therapy
  • Prednisolone:indicated if hypoxic with pO2< 9.3 kPa, to reduce the risk of respiratory failure (< 50% risk) and death
  • IV/ nebulised pentamidine:this is reserved for severe cases where co-trimoxazole is contraindicated or has failed
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108
Q

What is Bronchiectasis?

A

The permanent dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall

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109
Q

What can cause Bronchiectasis?

A

Anything that can cause chronic inflammation

  • Primary ciliary dyskinesia cilia don’t move properly cause bacteria to get caught in bronchi causing recurrent pneumonia
  • CF
  • Deficiency of bronchial wall elements
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110
Q

What are the symptoms of Bronchiectasis?

A
  • Inspiratory crackles
  • Wheezing
  • Productive cough
  • Large amounts of Khaki coloured sputum
  • SOB
  • Foul smelling mucus
  • Chest pain
  • Clubbing
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111
Q

What are the first-line investigations for Bronchiectasis?

A
  • CXR will show dilated airways with thickened walls that appear as tram tracks
  • Sputum cultures
  • Spirometry will show obstructive FEV1/FVC <0.7
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112
Q

What is the gold standard test for Bronchiectasis?

A

High resolution CT chest: shows bronchial dilation and bronchial wall thickening (Signet ring cell)

113
Q

What is cystic fibrosis?

A

An inherited autosomal recessive multi-system disease affecting the mucus glands

114
Q

A mutation on what gene causes CF?

A

cystic fibrosis transmembrane conductance regulatory gene on chromosome 7

115
Q

How does a mutation to the CFTR gene cause disease?

A
  • The CFTR protein gets misfolded and can’t migrate from the RER to the cell membrane
  • The CFTR is a channel protein that pumps chloride ions into various secretions helping to thin them out meaning secretions are left overly thick
116
Q

How does CF cause respiratory problems?

A
  • Results in dry airways and impaired mucociliary clearance
  • The low volume thick airway secretions result in reduced airway clearance increasing chances of infection and this chronic inflammation can lead to bronchiectasis
117
Q

What are the GI problems associated with CF?

A
  • Thickened secretions within small and large bowel can make it difficult to pass stools resulting in bowel obstruction
118
Q

What are the pancreatic problems associated with CF?

A

Thick pancreatic and bile secretions can block the pancreatic ducts resulting in a lack of digestive enzymes this can also result in pancreatitis and diabetes

119
Q

What are the liver problems associated with CF?

A

Thickened biliary secretions may block the bile ducts resulting in liver fibrosis and cirrhosis

120
Q

What are some other problems associated with CF?

A
  • Can result in pulmonary hypertension leading to right sided heart failure
  • In males there is bilateral absence of vas deferens so it means there is male infertility
121
Q

What if often the first sign of CF in a baby?

A

meconium ileus

122
Q

What is meconium ileus?

A
  • In babies the first stool passed is called the meconium and it is black and sticky and should be passed within 48 hours
  • In babies with CF the meconium does not pass as it is too sticky so it causes bowel obstruction occurs in 20% of babies with CF
123
Q

What are some signs of CF?

A
  • Low weight
  • Nasal polyps
  • Finger clubbing
  • Crackles and wheezes
  • Abdominal distension
124
Q

What are the symptoms of CF?

A
  • Chronic cough
  • Thick sputum production
  • Recurrent respiratory infections
  • Loose, greasy stools (steatorrhea) due to a lack of fat digesting lipase enzymes
  • Abdominal pain and bloating
  • Poor weight and height gain (failure to thrive)

-Parents may report the child tastes particularlysaltywhen they kiss them, due to the concentrated salt in the sweat

125
Q

When is CF most often diagnosed?

A
  • It is found during the heel-prick/Guthrie test which screens for CF in babies by looking for serum immunoreactivity trypsinogen
126
Q

What is the gold standard test for CF?

A

The sweat test

127
Q

What is the sweat test?

A

test for CF

  • Pilocarpine is applied to the skin and electrodes are placed either side of the patch with small current to cause skin to sweat
  • The sweat is absorbed and sent to lab for testing a diagnostic test of chloride concentration above **60 mmol/l is diagnostic
128
Q

What are common microbial colonisers in CF?

A
  • Staphylococcus aureus- patients take long term prophylactic flucloxacillin
  • Pseudomonas aeruginosa- can be harder to treat and worsen the prognosis
129
Q

what is the new miracle cure for CF?

A

Kaftrio, described by patient groups as a ‘revolutionary drug’, is a triple combination treatment combining three drugs which perform different functions – ivacaftor, tezacaftor and elexacaftor – and tackles the underlying causes of the disease, by helping the lungs work effectively.

130
Q

What is the management for the respiratory symptoms of CF?

A
  • Chest physiotherapy at least twice a day to remove mucus
  • Exercise
  • Salbutamol
  • Nebulised DNase (dornase alfa wolf) an enzyme that breaks down DNA material in respiratory secretions
  • Nebulised hypertonic saline
131
Q

What is the treatment for the GI symptoms of CF?

A
  • CREON tablets helps to digest fats in patients with pancreatic insufficiency (missing lipase)
  • High calorie diet to make up for malabsorption and calories needed for respiratory effort
132
Q

What is the prognosis for CF?

A

. Life expectancy is improving and currently the cystic fibrosis trust gives a median life expectancy of 47 years.

  • 90% of patients with CF develop pancreatic insufficiency
  • 50% of adults with CF develop cystic fibrosis-related diabetes and require treatment with insulin
  • 30% of adults with CF develop liver disease
    Most males are infertile due to absent vas deferens
133
Q

What is pleural effusion?

A

When fluid collects between the parietal and visceral pleural surfaces of the thorax

134
Q

What are the two types of pleural effusion?

A
  • Transudate= low protein count fluid moving across into the pleural space think of fluid shifting <30g/l
  • Exudate= high protein count caused by inflammation proteins leak out of tissues >30g/L
135
Q

What are the causes of transudative pleural effusion?

A
  • Congestive heart failure
  • Hypoalbuminemia
  • Hypothyroidism
  • Meig’s syndrome (right sided pleural effusion with ovarian malignancy)
136
Q

What are the causes of exudative causes of pleural effusion?

A

increased capillary permeability

  • Lung cancer
  • Pneumonia
  • Rheumatoid arthritis
  • TB
137
Q

What are the signs of pleural effusion?

A
  • Reduced chest expansion and reduced breath sounds on affected side
  • Dullness to percussion
  • Pleural friction rub (raspy breathing sound) in the superior aspect
  • Tracheal deviation away from the effusion
138
Q

What are the symptoms of pleural effusion?

A
  • SOB
  • Cough
  • Pleuritic chest pain
  • Symptoms of underlying cause
139
Q

What is the primary investigation for pleural effusion and what would it show?

A

Chest x-ray and it would show:
- Blunting to costophrenic angle
- Fluid in lung fissure
- Larger effusions will have a meniscus
- Tracheal and mediastinal deviation if it is a massive effusion

140
Q

What is the treatment for pleural effusion?

A
  • Conservative management
  • Pleural aspiration- involves sticking a needle in a aspirating the fluid however effusion may recur after this
  • Chest drain- can be used to drain effusion and prevent it from recurring
141
Q

What is a complication of pleural effusion?

A

Empyema where there is an infected pleural effusion

142
Q

When would you suspect empyema?

A

When a patient has an improving pneumonia but new or ongoing fever. Pleural aspiration will show pus, acidic pH <7.2 ,low glucose and high LDH.

143
Q

How is empyema treated?

A

Chest drain plus antibiotics

144
Q

What is a pneumothorax?

A

When air gets into the pleural space separating the lung from the chest wall.

Typical presentation is young tall, thing young man presenting with sudden shortness of breath and pleuritic chest pain whilst playing sports

145
Q

What are the causes of a pneumothorax?

A
  • Spontaneous
  • Trauma
  • Iatrogenic such as due to a lung biopsy
  • Lung pathology
146
Q

What causes a primary spontaneous pneumothorax?

A
  • No underlying disease due to spontaneous rupture of a subpleural bleb
147
Q

What are the risk factors for a primary spontaneous pneumothorax?

A
  • Tall
  • Smoking
  • Marfans
  • Rheumatoid
  • Diving or flying
148
Q

What is as secondary spontaneous pneumothorax?

A
  • Typical presentation is a middle aged patient with COPD presenting with a sudden onset of breathlessness and chest pain
149
Q

What is a tension pneumothorax and what causes it?

A
  • Typical presentation: a ventilated patient suddenly becomes breathless and haemodynamically unstable. This is an emergency
  • Air is forced into the thoracic cavity without means of escape it is a one way valve.
150
Q

Why is a tension pneumothorax dangerous?

A
  • Air is drawn in to the pleural space with each breath and cannot escape.
  • This is dangerous as it creates pressure in the thorax and will push the mediastinum across kinking the big vessels causing cardiorespiratory arrest
151
Q

What are the symptoms of a pneumothorax?

A
  • Sudden onset pleuritic chest pain
  • Sudden-onset dyspnoea
  • Sweating
152
Q

What are the signs of a pneumothorax?

A
  • Tachycardia
  • Cyanosis
  • Reduced breath sounds ipsilaterally
  • Hyper expansion (associated with tension pneumothorax)
  • Contralateral tracheal deviation (in a tension pneumothorax)
153
Q

What is the first line investigation for a pneumothorax?

A

-If tension pneumothorax is suspected then don’t wait

Chest x-ray would be first line and would show:
- no pleural edge with no lung markings
- Look for mediastinal shift in tension

154
Q

What is the gold standard investigation for a pneumothorax?

A

CT chest: will show an accurate size of the pneumothorax will be rarely used though

155
Q

What is the treatment for a spontaneous pneumothorax?

A
  • If no SOB and is smaller than 2cm then no treatment is required
  • If SOB and/or 2cm rim of air then it requires aspiration
  • If aspiration fails twice it will require a chest drain
156
Q

What is the management for a tension pneumothorax?

A
  • Initially inset a large bore cannula into the second intercostal space in the midclavicular line do not wait to do this
  • Once the pressure is relieved then use a chest drain
157
Q

Where are chest drains usually inserted?

A
  • The 5th intercostal space (or the inferior nipple line)
  • The mid axillary line (or the lateral edge of the latissimus dorsi)
  • The anterior axillary line (or the lateral edge of the pectoris major)
158
Q

What is the prognosis for a pneumothorax?

A

3.3% mortality

159
Q

What is interstitial lung disease?

A
  • An umbrella term to describe conditions that affect the lung parenchyma causing inflammation and fibrosis.
  • This means normal elastic and functional lung tissue is replaced with scar tissue that is stiff and does not function
160
Q

What is pulmonary fibrosis (PF)?

A

It describes the interstitial fibrosis of the lung parenchyma and has a number of causes. The most common cause is idiopathic

161
Q

What are some causes of drug induced PF?

A
  • Amiodarone
  • Cyclophosphamide
  • Methotrexate
  • Nitrofurantoin
162
Q

What are some causes of secondary PF?

A
  • Alpha-1 antitrypsin
  • Rheumatoid arthritis
  • SLE
  • Systemic sclerosis
  • Asbestosis (kind of it’s own thing but can’t be bothered to make another cad for it)
163
Q

What is hypersensitivity pneumonitis?

A
  • It is a type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction in people sensitive to that allergen. Some causes include:
  • Bird-fanciers lung
  • Farmers lung
  • Mushroom workers lung
  • Malt workers lung
  • Louis Ertl lung
  • Bronchoscopy will show raised lymphocytes and mast cells
164
Q

Describe the pathophysiology of idiopathic PF?

A
  • Type II Pneumocytes over-proliferate during repair process of the lungs leading to too many myofibroblasts and too much collagen
  • The myofibroblasts don’t undergo apoptosis and instead make even more collagen. As the collagen accumulates it thickens the intestinal layer between the alveoli and capillary leading to poor ventilation
  • Eventually the excess collagen causes the lungs to become stiff making it harder for air to flow in and out. It decreases TLC, FEV1 and FVC
165
Q

What is the pattern created by lung fibrosis called?

A

The loss of alveoli, creates cysts surrounded by thick walls this is called HONEYCOMBING

166
Q

What are the symptoms of idiopathic PF?

A
  • Progressive dyspnoea
  • Non-productive cough
  • Malaise
167
Q

What are the signs of idiopathic PF?

A
  • Bibasal fine end-inspiratory crackles
  • Clubbing
  • Cyanosis

It has an insidious onset

168
Q

What is the primary investigation for PF?

A

-High resolution CT scan of the thorax. It will show a ground glass/honeycomb appearance with interstitial lung disease

169
Q

What test is performed when CT scan is unclear for PF?

A

Lung biopsy

170
Q

What antibodies may be present in PF?

A

Antinuclear antibodies (ANA) and rheumatoid factor (RF):

ANA is positive in 30% and RF is positive in 10-20%, but this doesnotconfirm that the fibrosis is secondary to connective tissue disease

171
Q

What is the management for PF?

A
  • Remove/treat underlying cause
  • Home oxygen when hypoxic at rest
  • Stop smoking
  • Physiotherapy
  • Pneumococcal and flu vaccine
  • Advanced care planning and palliative care where appropriate
172
Q

What are some drugs that can slow the progression of IPF?

A
  • Pirfenidone is an antifibrotic and anti-inflammatory
  • Nintedanib is a monoclonal antibody targeting tyrosine kinase
173
Q

What is the prognosis for IPF?

A

IPF has a poor prognosis, with median survival ranging from 2.5 - 3.5 years after diagnosis.

Respiratory failure due to progressive disease is the most common cause of death. Most patients undergo subacute deterioration (worsening over > 4 weeks - months) before their death.

174
Q

What is sarcoidosis?

A
  • It is a granulomatous inflammatory multi-systemic disease where any organ can be affected but it predominately affects the lungs
175
Q

What are the risk factors for sarcoidosis?

A
  • Afro-Caribbean
  • Young adults
  • Female gender
  • Family history

young african american lady is standard question

176
Q

What would a typical presentation of sarcoidosis be?

A

A 20-40 year old black women presenting with a dry cough and shortness of breath. They may have nodules on their shins

177
Q

Describe the pathophysiology of sarcoidosis

A
  • It is a type IV hypersensitivity reaction against an unknown antigen. A T cell-mediated immune response to an antigenic stimulus attracts immune cells and causes the formation of granulomas
  • The granulomas in sarcoidosis are non-caseating meaning there is no tissue necrosis at the centre,
  • Macrophages fuse together to form a single large multi-nucleated cell called a Langhans giant cells.
178
Q

What are the pulmonary symptoms of sarcoidosis?

A
  • Mediastinal lymphadenopathy
  • Pulmonary fibrosis
  • Pulmonary nodules
  • Dry productive cough
  • Dyspnoea
179
Q

What are the signs of sarcoidosis on the skin?

A

Erythema nodosum
Lupus pernio (raised, purple skin lesions commonly on cheeks and nose)
- Granulomas develop in scar tissue

180
Q

What other organs are affected in sarcoidosis and what are the symptoms

A
  • Liver 20% (cirrhosis and nodules)
  • Eyes 20% (uveitis, conjunctivitis and optic neuritis)
  • Heart 5% (Heart blocks)
  • Kidney 5% (Kidney stones (due to hypercalcaemia)Nephrocalcinosis Interstitial nephritis)
181
Q

What are some syndromes associated with sarcoidosis?

A
  • Lofgren’s an acute form of sarcoidosis that is associated with polyarthritis, erythema nodosum and bilateral hilar lymphadenopathy
  • Heefordt’s syndrome causes facial nerve palsy fever, uveitis and parotitis
  • Mikulicz’s disease: bilateral parotid and lacrimal gland enlargement; can also occur due to TB and lymphoma.
182
Q

What are some differentials for sarcoidosis?

A
  • Tuberculosis
  • Lymphoma
  • Hypersensitivity pneumonitis
  • Toxoplasmosis
  • HIV
183
Q

What are the blood tests for sarcoidosis?

A
  • Raised serum ACE. Often used as a screening test
  • Hypercalcaemia is a key finding
  • Raised serum soluble interleukin 2 receptor
  • Raised CRP
184
Q

What would imaging for sarcoidosis show?

A
  • CXR would show hilar lymphadenopathy
  • High-resolution CT thorax shows hilar lymphadenopathy and pulmonary nodules
185
Q

What is the gold standard test for sarcoidosis?

A
  • Histology from a biopsy which is done using bronchoscopy with ultrasound guided biopsy.
186
Q

What would the histology of sarcoidosis show?

A

Non-caseating granulomas with epithelioid cells

187
Q

What is the treatment for sarcoidosis?

A
  • First line is corticosteroids, e.g. inhaled budesonide or oral prednisolone
  • Second line is immunosuppressants such as methotrexate and azathioprine
188
Q

What is pulmonary hypertesnion?

A

A mean pulmonary arterial pressure that is greater than 25 mmHg

189
Q

What are the group 1 causes of PHT?

A
  • Primary pulmonary hypertension
  • Connective tissue disease e.g. SLE
190
Q

What is the cause of group 2 PHT?

A

Left heart failure die to MI or systemic hypertension

191
Q

What is the cause of group 3 PHT?

A

Chronic lung disease such as COPD

192
Q

What is the cause of group 4 PHT?

A

Pulmonary vascular disease such as PE

193
Q

What is the cause of group 5 PHT?

A

Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorders

194
Q

What is cor pulmonale?

A
  • When high pressure in the pulmonary artery maker it harder for the right ventricle to pump blood and over time it causes hypertension.
  • When the right side of the heart becomes too big for oxygen supply causes right side heart failure. Known as cor pulmonary if caused by chronic lung disease
195
Q

What are the signs and symptoms of pulmonary hypertension?

A
  • SOB- main symptom
  • Chest pain
  • Syncope
  • Tachycardia
  • Hepatomegaly
  • Oedema
  • Raised JVP
196
Q

What changes would be show on an ECG for PHT?

A

Right sided heart strain can cause:

  • Right ventricular hypertrophy will show larger R waves on V1-3 and S waves on V4-6
  • Right axis deviation
  • Right bundle branch block
197
Q

What would a CXR show for PHT?

A

Dilated pulmonary arteries
Right ventricular hypertrophy

198
Q

What other tests would be performed for PHT?

A
  • A raised NT-proBNP blood test result indicates right ventricular failure
  • Echo can be used to estimate pulmonary artery pressure
199
Q

What is the management for primary PHT?

A
  • IV prostanoids epoprostenol
  • Endothelin receptor antagonists macitentan
  • Phosphodiesterase-5 inhibitorssildenafil
200
Q

What is the prognosis for PHT?

A

The prognosis is quite poor with a 30-40% 5-year survival from diagnosis. This can increase to 60-70% where specific treatment is possible.

201
Q

How common is lung cancer?

A

Third most common cancer behind breast and prostate

202
Q

What % of lung cancers are related to smoking?

A

Around 80% this includes other preventable causes

203
Q

What are the two main categories lung cancers are split in to?

A

Small cell- 20%
Non-small cell lung cancer- 80%

204
Q

What are the different types NSCLC?

A
  • Adenocarcinoma (40%)
  • Squamous cell (20%)
  • Large-cell carcinoma (10%)
205
Q

Describe the pathophysiology of SCLC?

A
  • A central lesion near the main bronchus. They are derived from neuroendocrine Kulchitsky cells
  • They contain neurosecretory granules that can release neuroendocrine hormones
  • They grow rapidly and patients present in an advanced stage
206
Q

What are the paraneoplastic syndromes that can be caused by SCLC?

A
  • SIADH causing hyponatremia
  • Ectopic ACTH causing Cushing’s
  • Lambert-Eatonmyasthenic syndrome
  • Limbic encephalitis- this causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.
207
Q

What is Lambert-eaton syndomre?

A
  • Antibodies produced against cancer cells damage voltage gated calcium channels sited on pre-synaptic terminals in motor neurones.
  • This leads to weakness in proximal muscles and can affects intraocular muscles causing double vison ptosis
  • Can also affect pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.
208
Q

Describe the pathophysiology of Squamous cell carcinomas

A
  • Location: central lesion
  • Cells produce keratin
  • They can cause hypercalcaemia by secretion of ectopic parathyroid hormone
209
Q

Describe the pathophysiology of adenocarcinomas

A
  • Location: peripheral lesion
  • Originate from mucus-secreting glandular cells
  • Can cause gynaecomastia
210
Q

Describe the pathophysiology of large cell carcinomas

A
  • Location: peripheral lesion commonly, but found throughout lungs
  • Lack both glandular and squamous differentiation
  • Can cause ectopic β-HCG secretion
211
Q

Describe the pathophysiology of carcinoid tumours

A

They can cause carcinoid syndrome which causes the secretion of hormones in particular serotonin which leads to increased peristalsis, diarrhoea and bronchoconstriction

212
Q

What are the signs and symptoms of lung cancer?

A
  • SOB
  • Cough
  • Haemoptysis
  • Finger clubbing
  • Recurrent pneumonia
  • Weigh loss
  • Lymphadenopathy – often supraclavicular nodes are the first to be found on examination
213
Q

What are some extrapulmonary signs and symptoms of lung cancer?

A
  • Fever
  • Night sweats
  • Hoarseness
  • Facial plethora and swelling due to SVC obstruction
214
Q

What is the first-line investigation and what will it show for lung cancer?

A

Chest x-ray will show:

  • Hilar enlargement
  • peripheral opacity
  • Bilateral pleural effusion
  • Collapse
215
Q

What is the gold standard investigation for lung cancer?

A

CT Chest, abdomen and pelvis with contrast.

216
Q

If CT is suggestive of malignancy what test is perfomed?

A
  • PET-CT the scan involves injecting a radioactive tracer and taking images using CT scanner and gamma ray detector.
  • It shows how metabolically active each tissue is and shows where tumour may have spread
217
Q

What is used to stage lung cancer?

A

TMN staging

218
Q

What is used to treat non-metastatic (stage I to IIIa) NSCLC?

A
  • Usually involves surgery with an adjuvant of chemotherapy
219
Q

What are the surgeries to treat NSCLC?

A
  • Lobectomy removing the lung lobe where the tumour is present
  • Segmentectomy or wedge resection
220
Q

What is used to relieve bronchial obstruction in lung cancer?

A

Endobronchial treatment with stents or debulking

221
Q

What is Horner’s syndrome?

A

Horner’s syndromeis a triad of partial ptosis, anhidrosis and miosis. It is caused by aPancoast’s tumour(tumour in thepulmonary apex) pressing on thesympathetic ganglion.

nb: dont confuse with horny syndrome, which tom coles has

222
Q

What is the prognosis for lung cancer?

A

Prognosis for lung cancer is poor, with a 10-year survival rate of 5.5%.

SCLC has a poorer prognosis than NSCLC, as SCLC patients will likely have disseminated disease at the point of first presentation.

223
Q

What is a mesotheliomas?

A

An aggressive epithelial neoplasm arising from the lining of the lung, abdomen, pericardium, or tunica vaginalis.

224
Q

What are the risk factors for a mesothelioma?

A
  • Increasing age
  • Male gender
  • Asbestos exposure
225
Q

How does asbestos cause a mesothelioma?

A
  • Cancer develops around 20-40 years after exposure. The asbestos fibres make their way to the mesothelium where they get tangled up with the cell’s chromosome
  • This causes DNA damage and modification in gene expression thus increasing the risk of cancer
226
Q

What is gold-standard for diagnosis in mesothelioma?

A

Thoracoscopy

227
Q

What is the prognosis for a mesothelioma?

A

The prognosis for mesothelioma is very poor, as only 5-10% of patients live beyond 5 years after their diagnosis. The median survival is only 12 months.

228
Q

What is used to asses the scale of dyspnoea?

A

The MRC dyspnoea scale

229
Q

What is the MRC dyspnoea scale?

A

It asses the degree of baseline functional disability due to dyspnoea.

Grade 0: only get breathless with strenuous exercise

Grade 1: get short of breath when hurrying or walking up hill

Grade 2: on ground level stop when walking at normal pace

Grade 3: stop for breath when walking 100 yards

Grade 4: too breathless to leave house

230
Q

What are the main causes of acute dyspnoea?

A
  • PE
  • Pneumothorax
  • Asthma
  • Pneumonia
231
Q

What are the causes reparatory failure?

A

Impaired ventilation:
- Neural problems
- COPD
- Asthma
- Pneumonia

Impaired perfusion
- Pulmonary hypertension
- Heart failure
- PE
- Shunt

Impaired gas exchange:
- Emphysema
- Pulmonary fibrosis

232
Q

What is type 1 respiratory failure?

A

When the respiratory system cannot provide adequately provide oxygen to the body

233
Q

What will type 1 respiratory failure show?

A

Type 1= 1 change (O2)
- pO2 (partial O2 pressure) is low
- pCO2 (partial CO2 pressure) is low or normal

234
Q

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

A

PE

235
Q

What is type 2 respiratory failure?

A

When the respiratory system cannot sufficiently remove carbon dioxide from the body leading to hypercapnia

236
Q

What is type 2 respiratory failure?

A

Type 2= 2 changes (O2 and CO2)
- pO2 (partial O2 pressure) is low
- pCO2 (partial CO2 pressure) is high

237
Q

What are the most common causes of type 2 respiratory failure?

A

Hypoventilation caused by:
COPD
Neuromuscular weakness
Obesity
Chest wall deformity
Reduced respiratory rate

238
Q

What are the signs of hypercapnia in type 2 respiratory failure?

A
  • Bounding pulse
  • Flapping tremor
  • Confusion
  • Drowsiness
  • Reduced consciousness
239
Q

What is DLCO a measure of?

A

Transfer Coefficient of oxygen/CO

Measure of ability of oxygen to diffuse across the alveolar membrane

240
Q

How is DLCO measured?

A

Can calculate by inspiring a small amount of carbon monoxide (not too much since can kill)
hold breath for 10 seconds at total lung capacity (TLC) then the gas transferred is measured

241
Q

What causes a high DLCO?

A

Pulmonary haemorrhage - can absorb O2 very efficiently due to bleeding resulting in more red blood cells being available

242
Q

What causes a low DLCO?

A
  • Severe emphysema
  • Fibrosing alveolitis
  • Anaemia
  • Pulmonary hypertension
  • Idiopathic pulmonary fibrosis
  • COPD
243
Q

What are the main URTI?

A
  • Epiglottis
  • Laryngitis
  • Pharyngitis
  • Sinusitis
  • Whooping cough
  • Croup
244
Q

What is pharyngitis?

A

Inflammation of the pharynx with exudate production

245
Q

What are the causes of pharyngitis?

A

Viral- EBV and adenovirus. (rhinovirus causes tonsillitis)

Bacteria- group A Strep (S.pyogenes)

246
Q

What are the signs of pharyngitis?

A
  • Sore throat
  • Fever
  • Cough
  • Nasal congestion (viral)
  • Exudate (bacterial)
247
Q

What must be ruled out if someone (especially a child) has pharyngitis?

A

Rheumatic fever (typically 2-4 weeks post S.pyogenes infection)

248
Q

What is the treatment for pharyngitis?

A
  • Viral is self-limiting
  • Bacterial- amoxicillin/flucloxacillin
249
Q

What causes sinusitis?

A

Viral infection (Rhinovirus, parainfluenza virus, and influenza virus) is the most common.

Can be caused by bacterial infection (Streptococcus pneumoniae, haemophilus influenzae and staphylococcus aureus)

250
Q

What is the treatment for viral sinusitis?

A
  • Self-limiting. Usually lasts <10 days and has a non purulent discharge
  • If no improvement after 10 days then give high dose steroid nasal spray
251
Q

What is the treatment for bacterial sinusitis?

A
  • May have a purulent discharge and last for longer than 10 days
  • If no improvement after 10 days and likely bacterial cause then give delayed or immediate antibiotics e.g. amoxicillin
252
Q

What is otitis media?

A

Infection and inflammation of the middle ear

253
Q

What are the causes of otitis media?

A

Bacteria- Streptococcus pneumoniae (most common), haemophilus influenzae, and staphylococcus aureus

Viral- Respiratory syncytial virus, rhinovirus, adenovirus

254
Q

What is the diagnostic finding for otitis media?

A

Otoscopy examination will reveal a bulging tympanic membrane

255
Q

What is the treatment for otitis media?

A
  • Will usually resolve within 3-7 days
  • Can give amoxicillin
  • 2nd line would be Co-amoxiclav
256
Q

What is acute epiglottitis?

A

Inflammation and localised oedema of the epiglottis which can result in life threating airway obstruction

257
Q

What is the most common cause of epiglotitis?

A
  • Caused by a bacterial infection of the epiglottis most commonly by Haemophilus influenzae B(gram-negative coccobacillus) in children.
258
Q

Why have incidence of epiglottitis decreased?

A

The introduction of the HiB vaccination has caused numbers to fall

259
Q

What are the risk factors for epiglottitis?

A
  • Peak age 6-12
  • Male gender
  • Unvaccinated
  • Immunocompromised
260
Q

What are the signs of epiglottitis?

A
  • Stridor
  • Muffled voice
  • Respiratory distress
  • Tripod position (the patient leans forward and supports their upper body with their knees)
  • Fever
261
Q

What are the symptoms of epiglottitis?

A
  • Fever
  • Sore throat
  • Dysphagia
  • Dysphonia
  • Drooling
  • Distress
262
Q

What is the primary investigation of epiglottitis?

A

DO NOT examine the airway or distress the child as this could lead to catastrophic airway occlusion and respiratory arrest

  • Laryngoscopy- will show swelling and inflammation of the epiglottis or supraglottis
  • Lateral neck radiography- secure the airway first but look for thumb sign on trachea useful for ruling out foreign body
263
Q

What is the treatment for epiglottitis?

A

First line:
- Secure airway
- Nebulised adrenaline
- IV antibiotics

Second line:
Dexamethasone

264
Q

What is croup?

A

Acute infective upper respiratory infection causing oedema in the larynx

265
Q

Who is typically affected by croup?

A

Children between 6 months and 2 years old

266
Q

What are the causes of Croup?

A

Main cause : Parainfluenza virus

Influenza
Adenovirus
Respiratory syncytial virus

267
Q

What are the signs of croup?

A
  • Pyrexia
  • Stridor
  • Respiratory distress
268
Q

What are the symptoms of croup?

A
  • Barking cough worse at night
  • Difficulty breathing
  • Fever
  • Coryza (inflammation of the nose) basically a blocked nose
269
Q

What is used to classify the severity of croup?

A
  • Most often a clinical diagnosis is made

-The Westley score is a classification system used to asses the severity

270
Q

What is the treatment for croup?

A

Oral dexamethasone (single dose 150mcg/kg)

271
Q

What is whooping cough?

A

URTI caused by Bordetella pertussis

272
Q

Who is affected by whooping cough?

A

Mainly children 90% are under 5

273
Q

What are the the stages of whooping cough?

A

Catarrhal stage (1-2 weeks)

Paroxysmal stage (1-6 weeks)

Convalescent stage (lasts up to 6 months)

274
Q

What is the catarrhal stage of whooping cough?

A
  • Dry unproductive cough
  • Low grade fever
  • Conjunctivitis
  • Coryzal symptoms
275
Q

What is the paroxysmal of whooping cough?

A
  • Coughing fits: typically consist of a short expiratory burst followed by an inspiratory gasp, causing the ‘whoop’ sound
  • Post-tussive vomiting
276
Q

What is the characteristic symptom of whooping cough?

A

Whoop sound caused by sharp inhalation of breath after coughing bout

277
Q

What are the investigations for whooping cough?

A

Nasopharyngeal swab/aspirate: culture/PCR

Anti-pertussis toxin IgG

278
Q

What is the treatment of whooping cough?

A

Notify PHE

  • Antibiotics marcolids clarithromycin or azithromycin
  • Stay off school as highly contagious
279
Q

What are the complications of whooping cough?

A
  • Pneumonia
  • Encephalopathy
  • Otitis media
  • Injuries from coughing e.g., pneumothorax and seizures

Phase 2A Tom (15 decks)

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