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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is asthma?

A

a chronic inflammatory airway disease characterised by reversible, intermittent airway obstruction and hyper-reactivity

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2
Q

What makes up the atopic triad?

A

Asthma
Hayfever
Eczema

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3
Q

What is occupational asthma?

A

asthma caused by environmental triggers in the workplace

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4
Q

What is the aetiology of asthma and when does it typically present?

A

gentic predispostion + environmental trigger
typically presents in childhood but can be adult onset

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5
Q

What are the main features of asthma?

A

Episodic + diurnal variability: symptoms fluctuate at different times of the day, typically worse at night
SOB
Chest tightness
Dry cough
Wheeze
should improve with bronchodilators
may have family hx or hx of eczema, hay fever, food allergies

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6
Q

What are some potential triggers for asthma?

A
  • Infection
  • Nighttime or early morning
  • Exercise
  • Animals
  • Cold, damp or dusty air
  • Strong emotions
  • Beta-blockers, NSAIDs
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7
Q

What are the risk factors for asthma?

A

family hx
allergens/irritants
atopic disease hx
cigarette smoking/ vaping
respiratory viral infection early in life
nasal polyposis
low socioeconomic status

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8
Q

What is the pathophysiology of an asthma exacerbation?

A

Early phase
- Excess of T helper 2 cells (type 2 inflammation)
- TH2 cells produce IL4, IL13 and IL5
- IL4+13 cause plasma cells to release IgE which activate mast cell degranulation
- Histamine, leukotriene and prostaglandins (T1 hypersensitivity reaction)
- Bronchospasm, increased mucus production and oedema Late phase
- More inflammatory cells recruited from blood (chemotaxis)
- Second phase of exacerbation

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9
Q

What are some of the long term consequences of asthma?

A

subepithelial fibrosis
basement membrane thickening
hypertrophy of smooth muscle cells
larger volume of mucus
increased vascularity

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10
Q

What is the forced expiratory volume in 1 second (FEV1) spirometry test and what does it measure?

A

the air a person can forcefully exhale in 1 second.
This measures how easily air can flow out of the lungs.
It is reduced with airflow obstruction

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11
Q

What is reversibility testing?

A

involves giving a bronchodilator (e.g., salbutamol) before repeating the spirometry to see if this impacts the results

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12
Q

What is the FEV1/FVC ratio for obstructive lung disease?

A

FEV1:FVC ratio of less than 70%.

person may have a relatively good lung volume, but air can only move slowly in and out of the lungs due to obstruction

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13
Q

What are FEV1 and FVC like in restrictive airway disease?

A

FEV1 and FVC are equally reduced
FEV1:FVC ratio greater than 70%

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14
Q

What is restrictive lung disease?

A

limits the ability of the lungs to expand and fill with air.
The lungs are restricted from effectively expanding

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15
Q

Difference in spirometry for restrictive and obstructive?

A

a low FVC indicates restrictive lung disease
a low FEV1:FVC ratio (under 70%) indicates obstructive lung disease

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16
Q

What does peak flow measure?

A

measures the “peak”, or fastest point, of the expiratory flow of air
a simple way of demonstrating how much obstruction to airflow is present in the lungs
and how well a condition such as asthma is controlled

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17
Q

What is PaO2?

A

partial pressure of oxygen, the amount of oxygen dissolved in the blood.
A low PaO2 indicates hypoxia.

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18
Q

What is FiO2?

A

fraction of inhaled oxygen.
Room air has an FiO2 of 21%, meaning the oxygen conc in room air is 21%

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19
Q

What investigations should be done for a patient presenting with suspected asthma?

A

Spirometry: FEV1/FVC ratio <70%
BDR test (reversibility): improvement in FEV₁ of 12% or more in response to beta agonists
peak expiratory flow rate (PEFR)
FeNO
CXR
FBC with differential

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20
Q

What are some differentials for asthma?

A

COPD
Chronic rhinosinusitis
CHF
Bronchiectasis
CF

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21
Q

What is the first-line management of asthma?

A

Short-acting beta agonist: salbutamol inhaled: (100 micrograms/dose inhaler) 100-200 micrograms inhaled up to four times daily – as needed, reliever

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22
Q

What can be used in the management of asthma if a SABA isn’t effective alone?

A
  • Inhaled corticosteroid (ICS) beclometasone
  • Long-acting beta 2 agonist (formoterol) inhaled + ICS
  • Leukotriene receptor antagonists (montelukast)
  • Long acting muscarinic antagonists, e.g. tiotropium
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23
Q

How do beta-2 adrenergic receptor agonists work?

A

bronchodilators
Adrenalin acts on the smooth muscle of the airways to cause relaxation
Stimulating the adrenalin receptors dilates the bronchioles and reverses the bronchoconstriction present in asthma

SABAs work for a few hours, e.g. salbutamol

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24
Q

How do inhaled corticosteroids work?

A

reduce the inflammation and reactivity of the airways.
These are used as maintenance or preventer medications to control symptoms long-term and are taken regularly, even when well.

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25
Q

What are the presenting features of an acute asthma exacerbation?

A

Progressively shortness of breath
Use of accessory muscles
Raised respiratory rate (tachypnoea)
Symmetrical expiratory wheeze on auscultation
The chest can sound “tight” on auscultation, with reduced air entry throughout

initial resp alkalosis

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26
Q

What is a moderate acute asthma exacerbation defined as?

A

Peak flow 50 – 75% best or predicted

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27
Q

What is a severe acute asthma exacerbation defined as?

A

Peak flow 33-50% best or predicted
Respiratory rate above 25
Heart rate above 110
Unable to complete sentences

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28
Q

What is a life-threatening acute asthma exacerbation defined as?

A

Peak flow less than 33%
Oxygen saturations less than 92%
PaO2 less than 8 kPa
Becoming tired
Confusion or agitation
No wheeze or silent chest
Haemodynamic instability (shock)

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29
Q

What is silent chest?

A

wheeze disappears when the airways are so tight that there is no air entry

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30
Q

What can be used to manage an acute asthma exacerbation?

A
  • O2 therapy
  • Nebulised salbutamol or ipratropium bromide
  • Systemic corticosteroids: prednisolone
  • IV magnesium sulfate
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31
Q

How can asthma attacks be prevented?

A

Daily inhaled corticosteroids
Avoidance of known triggers

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32
Q

What are the possible complications of asthma?

A

COPD from airway remodelling
Acute exacerbations
Oral/ oesophageal candidiasis secondary to use of ICS
dysphonia secondary to use of ICS

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33
Q

What are the main features of a life threatening acute asthma attack?

A CHEST

A

Arrhythmia/ Altered conscious level
Cyanosis, PaCO2 normal
Hypotension, Hypoxia (PaO2<8kPa, SpO2 <92%)
Exhaustion
Silent chest
Threatening PEF < 33% best or predicted (in those >5yrs old)

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34
Q

How is a life threatening asthma attack managed?

O SHIT MI pneumonic

A

Oxygen
Salbutamol
Hydrocortisone (Prednisolone)
Ipratropium bromide
Theophylline
Magnesium sulphate
Intubation and ventilation

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35
Q

What is bronchiectasis?

A

Permanent, abnormal dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall

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36
Q

What can cause bronchiectasis?

A

Post infectious: childhood, mycobacteria, pneumonia, COVID
COPD
Asthma
Connective tissue disorders (RA, Sjogrens)
Allergic bronchopulmonary aspergillosis
Genetic: CF
Immunodeficiency
Yellow nail syndrome

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37
Q

What is the pathophysiology of bronchiectasis?

A

dilation and thickening of the bronchi due to chronic inflammation in response to micro-organisms colonising the airways.
Persistent airway inflammation leads to bronchial wall oedema and increased mucus production
Inflammation leads to progressive destruction of airways, which serves as a nidus for subsequent airway colonisation
Vicious cycle of progressive damage and recurrent infections

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38
Q

What can be heard on auscultation for bronchiectasis?

A

Crackles
High-pitched inspiratory squeaks
Rhonchi
Wheezing

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39
Q

What investigations and imaging can be done for bronchiectasis?

A

CXR: Tram-track opacities, ring shadows
FBC
Sputum culture and sensitivity
High-resolution chest CT: thickened, dilated airways, varicose constrictions, cysts and/or tree-bud pattern

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40
Q

What are the symptoms of bronchiectasis?

A

Recurrent pulmonary infections
Chronic daily productive cough with mucopurulent sputum production
SOB
Weight loss
Fever
Fatigue
Rhinosinusitis

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41
Q

How does an acute exacerbation of bronchiectasis present?

A

worsening of cough
change in sputum colour
increase in sputum volume
fever
fatigue

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42
Q

What is the general management for bronchiectasis?

A
  • Exercise and nutrition
  • Vaccines (e.g., pneumococcal and influenza)
  • Respiratory physiotherapy to help clear sputum
  • Pulmonary rehabilitation
  • Long-term abx for frequent exacerbations (e.g., 3 or more per year)
  • Inhaled colistin for Pseudomonas aeruginosa colonisation
  • Long-acting bronchodilators for breathlessness
  • Long-term oxygen therapy in reduced oxygen saturation
  • Surgical lung resection may be considered for specific areas of disease
  • Lung transplant is an option for end-stage disease
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43
Q

What is the abx of choice for exacerbations caused by Pseudomonas aeruginosa?

A

Ciprofloxacin

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44
Q

What are some signs of bronchiectasis?

A

Finger clubbing
Signs of cor pulmonale (e.g., raised JVP and peripheral oedema)
Scattered crackles throughout the chest that change or clear with coughing
Scattered wheezes and squeaks

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45
Q

What is COPD?

A

Persistent, irreversible limitation of airflow through the lungs

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46
Q

In COPD, what is chronic bronchitis?

A

long-term symptoms of a cough and sputum production due to inflammation in the bronchi

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47
Q

In COPD what is emphysema?

A

damage and dilatation of the alveolar sacs and alveoli, decreasing the surface area for gas exchange

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48
Q

What is the epidemiology of COPD?

A

more common in older people, especially aged 65 years+
COPD prevalence is highest in the WHO region of the Americas and lowest in the South-East Asia and Western Pacific regions.
The pooled global prevalence is 15.7% in men and 9.93% in women

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49
Q

What causes COPD?

A

Exposure to inhaled toxins, i.e. smoking (up to 70% of cases), air pollution, occupational exposure
Genetic: alpha 1 antitrypsin deficiency

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50
Q

What is the pathophysiology causing loss of elastic recoil in COPD?

A

Inflammation due to exposure from inhaled toxins, e.g. cigarettes
Neutrophils and macrophages recruited and secrete proteases
Excess protease activity causing destruction of lung tissue
Loss of support for alveolar leading to reduced elastic recoil and emphysema

Reduced structural support causes collapse of smaller airways and trapped air, hyperinflation

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51
Q

What is the pathophysiology causing narrowing of the airways in COPD?

A

Inflammation increases oxygen free radicals, causing mucosal oedema, mucous hypersecretion and bronchoconstriction
Airways are narrower and have increased resistance to airflow
Fibrosis and irreversible

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52
Q

In COPD, what does the loss of elastic recoil and airway narrowing lead to?

A

impaired mucocilliary clearance and increase in the work of breathing
Reduced alveolar ventilation, hypoxia, hypercapnia

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53
Q

What are the grades 1-5 of the MRC dyspnoea scale?

A

Grade 1: Breathless on strenuous exercise
Grade 2: Breathless on walking uphill
Grade 3: Breathlessness that slows walking on the flat
Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
Grade 5: Unable to leave the house due to breathlessness

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54
Q

What might be present on physical exam of a COPD patient?

A

tachypnoea
respiratory distress
use of accessory muscles
intercostal retraction
Barrel chest
hyper-resonance on percussion
distant breath sounds and poor air movement

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55
Q

What symptoms may be present in COPD?

A

Dyspnoea- persistent and worsening, initially worse with exercise
Cough (commonly producing sputum)
Tachypnoea and use of accessory muscles
frequent bronchitis and recurrent infections
wheeze
waking at night with breathlessness
cyanosis
cor pulmonale
fatigue

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56
Q

What are the risk factors for COPD?

A

cigarette smoking
advanced age
genetic factors
lung growth and development

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57
Q

What are GOLD stages 1-4 of severity using post-bronchodilator FEV1 in COPD?

A

Stage 1 (mild): FEV1 more than 80% of predicted
Stage 2 (moderate): FEV1 50-79% of predicted
Stage 3 (severe): FEV1 30-49% of predicted
Stage 4 (very severe): FEV1 less than 30% of predicted

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58
Q

What physiological abnormalities are seen in COPD?

A

mucous hypersecretion
ciliary dysfunction
airflow obstruction
hyperinflation
gas exchange abnormalities
pulmonary HTN

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59
Q

What are the 3 groups (a,b,e) in the management of COPD?

A

Group A: low symptom burden and 0-1 exacerbations per year
Group B: increased symptom burden but still 0-1 exacerbations per year
Group E: 2 or more exacerbations per year

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60
Q

What is the initial pharmacological treatment for group A COPD?

0-1 exac, CAT less than 10

A

SABA or LABA (salbutamol or formoterol), SAMA or LAMA (ipratropium or tiotropium) – long acting more commonly used

a bronchodilator

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61
Q

What is the pharmacological treatment for group B COPD?

0-1 exac, CAT over 10

A

LABA/LAMA
glycopyrronium/formoterol

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62
Q

What is the pharmacological treatment for group E COPD?

2 or more exac or 1 hospital exac

A

1st line: LABA/LAMA
2nd line: LABA/LAMA + ICS
glycopyrronium and budesonide/formoterol inhaled

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63
Q

Apart from BA and MA, what other pharmacological treatments are available for COPD?

A
  • Mucolytics: carbocisteine
  • Systemic prednisolone in acute exacerbations
  • Roflumilast (diarrhoea side effects)
  • Azithromycin (abx 3x a week to reduce inflammation)
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64
Q

What are non-pharmacological treatment options for COPD?

A

Smoking cessation
Pulmonary rehabilitation
Vaccination

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65
Q

What are the differentials for COPD?

A

Asthma
Congestive heart failure
Bronchiectasis
Tuberculosis
Bronchiolitis
Upper airway dysfunction

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66
Q

What investigations can be done for COPD?

A

Post-bronchodilator spirometry: FEV1:FVC ratio of less than 70%
CXR: flattened diaphragm, hyperinflation
Pulse oximetry: low
FBC checking for: polycythaemia (haematocrit >55%), anaemia, and leucocytosis

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67
Q

What are the treatment options for an acute exacerbation of COPD?

A
  • SABA, e.g. salbutamol inhaled or nebulised
  • Short-acting muscarinic antagonist, e.g. ipratropium bromide
  • Target O2 sats of 88-92% (excess oxygen may suppress drive for ventilation and precipitate hypercapnia and type 2 resp failure)
  • Corticosteroid: pred or hydrocortisone
  • Non-invasive ventilation
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68
Q

What investigations are done for an acute exacerbation of COPD?

A

ABG
CXR
ECG
FBC
Inflammatory markers
Sputum culture

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69
Q

What are the target oxygen sats for patients with COPD at risk of retaining CO2?

A

88-92%

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70
Q

What is the risk of oxygen therapy in COPD?

A

Many patients with COPD retain CO2 when treated with oxygen, (oxygen-induced hypercapnia).

likely involves ventilation-perfusion mismatch and haemoglobin binding less well to CO2 when also bound to oxygen

hypoxic drive theory may not be right

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71
Q

What are some of the complications of COPD?

A

Exacerbations
Pulmonary HTN
Ptx
cor pulmonale
lung cancer
recurrent pneumonia
depression
respiratory failure
Anaemia
polycythaemia

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72
Q

What are the most common causes of acute dyspnoea in ED?

A

Asthma
COPD
Heart failure
Pneumonia

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73
Q

What the 5 aetiological categories causing dyspnoea?

A

Pulmonary disease
Cardiovascular disease
Respiratory muscle dysfunction
Psychogenic dyspnoea
Deconditioning/obesity.

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74
Q

What are the key physiological consequences of CF?

A

Thick pancreatic and biliary secretions that cause blockage of the ducts, resulting in a lack of digestive enzymes such as pancreatic lipase in the digestive tract

Low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections

Congenital bilateral absence of the vas deferens in males

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75
Q

How does CFTR mutation affect cells?

A

CFTR gene on chromosome 7 mutation.
Decreased secretion of chloride out of cells, increased resorption of sodium, more water in cell
Sticky, thick mucus

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76
Q

What is cystic fibrosis?

A

an autosomal recessive genetic condition affecting mucus glands resulting from mutations in CFTR channel

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77
Q

What causes CF?

A

Autosomal recessive
Mutations in the CFTR gene on chromosome 7
most common is the delta-F508 mutation

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78
Q

What are the risk factors for CF?

A

family hx of CF
known carrier status of both parents
white ethnicity

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79
Q

What are the symptoms of CF?

A

Chronic cough
Thick sputum production
Recurrent respiratory tract infections
Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes
Abdo pain and bloating
Failure to thrive
Meconium ileus in newborns

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80
Q

What investigations should be done for CF?

A

screened for at birth with the newborn bloodspot test
genetic testing
sweat test

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81
Q

How does the sweat test work in CF?

A

Pilocarpine and electrodes attached to skin
Small current passed over causing skin to sweat
sweat collected on gauze
sweat chloride ≥60 mmol/L

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82
Q

What are the main colonisers in CF? And how are they treated?

A

staph aureus and pseudomonas aeruginosa
pseudomonas: long term nebulised abx, e.g. tobramycin or oral ciprofloxacin
s.aureus prevention: long term prophylactic flucloxacillin

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83
Q

How is CF managed?

A

Chest physiotherapy several times a day is essential to clear mucus and reduce the risk of infection and colonisation
Exercise improves respiratory function and reserve, and helps clear sputum
High calorie diet
CREON tablets to digest fats in patients with pancreatic insufficiency
Treat chest infections when they occur
Bronchodilators can help treat bronchoconstriction
Nebulised DNase (Mucolytic)
Nebulised hypertonic saline
Vaccinations including pneumococcal, influenza and varicella

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84
Q

What should CF patients be screened for?

A

diabetes, osteoporosis, vitamin D deficiency and liver failure

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85
Q

What are the 2 types of pleural effusion?

A

Exudative – a high protein content (more than 30g/L)
Transudative – a lower protein content (less than 30g/L)

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86
Q

What is a pleural effusion?

A

a collection of fluid in the pleural space between parietal and visceral pleura in the thorax

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87
Q

What can cause an exudative pleural effusion?

A

malignancy
pleural infection
PE
autoimmune pleuritis

as a result of inflammation

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88
Q

What can cause a transudative pleural effusion?

A

Congestive cardiac failure
Hypoalbuminaemia
Cirrhosis
Meigs syndrome

fluid moving across or shifting into the pleural space

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89
Q

What are the risk factors for a pleural effusion?

A

CHF
Pneumonia
Malignancy
Recent CABG

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90
Q

What is present on a physical exam for a pleural effusion?

A

Dullness to percussion over the effusion
Reduced breath sounds
Tracheal deviation away from the effusion in very large effusions

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91
Q

What is seen on a CXR for a pleural effusion?

A

Blunting of the costophrenic angle
Fluid in the lung fissures
Larger effusions will have a meniscus
Tracheal and mediastinal deviation away from the effusion in very large effusions

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92
Q

What investigations should be done for a pleural effusion?

A

CT and ultrasound
Pleural fluid analysis
CXR

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93
Q

How might a pleural effusion present?

A

dullness to percussion
dyspnoea
cough
pleuritic chest pain

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94
Q

What is empyema?

A

infected pleural effusion

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95
Q

What is a pneumothorax?

A

When air gains access to, and accumulates in, the pleural space

96
Q

What can cause a pneumothorax?

A

Spontaneous
Trauma
Iatrogenic
Lung pathologies such as infection, asthma or COPD

97
Q

What are the risk factors of a ptx?

A

cigarette smoking
family hx of pneumothorax
tall and slender body build
age <40 years
recent invasive medical procedure
chest trauma
acute severe asthma
COPD
TB
CF

98
Q

What are the signs of a tension ptx?

A

ipsilateral reduced breath sounds
reduced chest expansion
hyper-resonance on percussion
tracheal shift to the contralateral side
Cardiopulmonary deterioration
- Hypotension
- Respiratory distress
- Low oxygen saturations
- Tachycardia
- Shock
- Loss of consciousness

99
Q

What are the symptoms of a ptx?

A

Severe pleuritic chest pain
Sweating
Dyspnoea

100
Q

What is used to diagnose a ptx?

A

Erect PA CXR
Chest ultrasound if cxr not possible

101
Q

What are some differentials of a pneumothorax?

A

Asthma, acute exacerbation
COPD, acute exacerbation
PE
MI
Pleural effusion

102
Q

How is a ptx treated?

A

High flow oxygen
Immediate decompression

103
Q

What is interstitial lung disease?

A

many conditions that cause inflammation and fibrosis of the lung parenchyma

104
Q

How can the interstitial lung diseases be diagnosed?

A

Clinical features
High-resolution CT scan of the thorax
Spirometry - restrictive

105
Q

What is idiopathic pulmonary fibrosis?

A

progressive pulmonary fibrosis with no apparent cause

manifests over several years
characterised by the formation of scar tissue within the lungs and progressive dyspnoea

prognosis is poor, with a 2-5 years life expectancy from diagnosis

106
Q

What is the epidemiology of IPF?

A

prevalence increases with advancing age
mean age at diagnosis of between 60 and 70 years
more common among men than among women

rare, but of the ILDs common

107
Q

What’s the pathophysiology of idiopathic pulmonary fibrosis?

A

injury triggers a pro-inflammatory and pro-fibrotic response that includes an influx of macrophages, fibroblasts, and other inflammatory cells.
Dysregulation of the normal tissue repair process.
Formation of fibroblastic foci, continued deposition of extracellular matrix (ECM) proteins, and progressive fibrosis

108
Q

What are the risk factors for IPF?

A

Family hx
cigarette smoking
advanced age
male sex

109
Q

How does IPF present?

A

insidious onset of SOB and dry cough over more than 3 months
Bibasal fine end-inspiratory crackles
Finger clubbing

110
Q

What does imaging for IPF show?

A

CXR: basilar, peripheral, bilateral, asymmetrical, reticular opacities
High-res CT: basilar- and subpleural-predominant areas of increased reticulation, honeycombing

111
Q

What investigations should be done for IPF?

A

CXR
HRCT
Pulmonary function tests showing restrictive
Surgical lung biopsy
ANA and RF

112
Q

What are the differentials of IPF?

A

Drug-related pulmonary fibrosis
Asbestosis
Hypersensitivity pneumonitis
Sarcoidosis
Pneumonia

113
Q

What’s the management for IPF?

A

Antifibrotic therapy: oral pirfenidone
Smoking cessation
Pulmonary rehabilitation
Oxygen therapy

114
Q

What are the possible complications of IPF?

A

Pulmonary htn
GORD
Pulmonary infection

115
Q

What can cause secondary pulmonary fibrosis?

A

Alpha-1 antitrypsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis
Sarcoidosis

116
Q

Which drugs can cause pulmonary fibrosis?

A

Amiodarone (antiarrhythmic, also causes grey/blue skin)
Cyclophosphamide(scleroderma)
Methotrexate (DMARD)
Nitrofurantoin (UTI)

117
Q

What is asbestosis?

A

lung fibrosis related to asbestos exposure

118
Q

How is asbestos damaging?

A

Fibrinogenic
Oncogenic

119
Q

What can asbestos inhalation cause?

A

Lung fibrosis
Pleural thickening and pleural plaques
Adenocarcinoma
Mesothelioma

120
Q

What is sarcoidosis?

A

a chronic granulomatous disorder of unknown aetiology
characterised by accumulation of lymphocytes and macrophages and the formation of non-caseating granulomas in the lungs and other organs

121
Q

What are granulomas?

A

inflammatory nodules full of macrophages

122
Q

Where does sarcoidosis most typically affect?

A

lungs, skin, and eyes

123
Q

What are the risk factors for sarcoidosis?

A

age 20-50 years
family history of sarcoidosis
Scandinavian origin
female

124
Q

What are the pulmonary symptoms of sarcoidosis?

A
  • cough and dyspnoea
  • Mediastinal lymphadenopathy
  • Pulmonary fibrosis
  • Pulmonary nodules
  • wheezing
125
Q

What are the extrapulmonary symptoms of sarcoidosis? (systemic, eyes, skin)

A

Systemic symptoms:
- fever
- fatigue
- weight loss

Eyes
- uveitis: red painful eyes, blurred vision
- conjunctival nodules

Skin
- erythema nodosum
- lupus pernio

126
Q

What are the extrapulmonary symptoms of sarcoidosis? (msk, neuro, heart)

A

MSK
- arthralgia and arthritis

Neuro
- facial nerve palsy
- pituitary involvement

Heart
- arrhythmias
- heart block
- chest wall pain

127
Q

What is Lofgren’s syndrome?

A

a specific presentation of sarcoidosis with a classic triad of symptoms:
Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)

128
Q

What are the differentials for sarcoidosis?

A

TB
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis

129
Q

What are the investigations for sarcoidosis?

A

CXR: bilateral hilar and right paratracheal adenopathy
spirometry: may show a restrictive defect
tissue biopsy: non-caseating granulomas
FBC: anaemia; leukopenia
Serum calcium: elevated
Serum ACE: elevated

130
Q

What would be seen on histology for sarcoidosis?

A

non-caseating granulomas with multi-nucleated giant cells in the centre

131
Q

What are the radiographic stages of pulmonary sarcoidosis?

A

Stage 0: normal
Stage I: bilateral hilar lymphadenopathy
Stage II: bilateral hilar lymphadenopathy plus pulmonary infiltrates
Stage III: pulmonary infiltrates without hilar lymphadenopathy
Stage IV: extensive fibrosis with distortion

132
Q

How is sarcoidosis managed?

A

Conservative management is considered in patients with no or mild symptoms.
Oral steroids
Bisphosphonates protect against osteoporosis whilst on long-term steroids.
Methotrexate is a second-line option.

133
Q

What is pulmonary hypertension?

A

Increased resistance and pressure in the pulmonary arteries
Causes strain on the right side of the heart as it tries to pump blood through the lungs.
Leads to back pressure through the right side of the heart and into the systemic venous system.

mean pulmonary arterial pressure of more than 20  mmHg.

134
Q

What are the causes of pulmonary htn?

A

Group 1 – Idiopathic pulmonary hypertension or connective tissue disease (SLE)
Group 2 – Left heart failure, MI or HTN
Group 3 – Chronic lung disease
Group 4 – Pulmonary vascular disease (PE)
Group 5 – Misc causes such as sarcoidosis, glycogen storage disease and haematological disorders

135
Q

What are the risk factors for pulmonary hypertension?

A

female sex
BMPR2 mutations
appetite suppressants
family hx

136
Q

What are the symptoms of pulmonary htn?

A

SOB
Syncope (loss of consciousness)
Tachycardia
Raised jugular venous pressure (JVP)
Hepatomegaly
Peripheral oedema

accentuated pulmonic component (P2) to the second heart sound
tricuspid regurgitation murmur

137
Q

What investigations should be done for pulmonary htn?

A

CXR: Dilated pulmonary arteries, RVH
ECG: RVH, right axis deviation, right atrial enlargement
transthoracic Doppler echocardiography
Raised NT‑proBNP

138
Q

What is the management for idiopathic pulmonary hypertension?

A

CCBs
IV prostaglandins (e.g., epoprostenol)
Endothelin receptor antagonists (e.g., macitentan)
Phosphodiesterase-5 inhibitors (e.g., sildenafil)

139
Q

What are the complications of pulmonary hypertension?

A

right ventricular failure
supraventricular tachyarrhythmias
treatment-related headache
central venous catheter-related infections

140
Q

What are occupational lung disorders?

A

lung conditions that have been caused or made worse by long-term exposure to certain irritants in the workplace

141
Q

What is sinusitis?

A

inflammation of the paranasal sinuses in the face
usually accompanied by inflammation of the nasal cavity and can be referred to as rhinosinusitis

142
Q

What can cause sinusitis?

A

Infection, e.g. following viral URTIs
Allergies, such as hayfever (with allergic rhinitis)
Obstruction of drainage
Smoking

143
Q

How does sinusitis present?

A

Nasal congestion
Nasal discharge
Facial pain or headache
Facial pressure
Facial swelling over the affected areas
Loss of smell

acute less than 12 weeks

144
Q

What are the management options for chronic sinusitis?

A

Saline nasal irrigation
Steroid nasal sprays or drops (e.g., mometasone or fluticasone)
Functional endoscopic sinus surgery (FESS)

145
Q

What is otitis media?

A

infection in the middle ear

146
Q

How does otitis media occur?

A

Bacteria enter from the back of the throat through the eustachian tube
A viral upper respiratory tract infection often precedes bacterial infection of the middle ear

147
Q

What are the symptoms of otitis media?

A
  • Ear pain
  • Reduced hearing in the affected ear
  • Feeling generally unwell, for example with fever
  • Symptoms of an upper airway infection
148
Q

Which bacteria most commonly causes otitis media?

A

streptococcus pneumoniae

149
Q

What is epiglottitis?

A

inflammation and swelling of the epiglottis
can swell to the point of completely obscuring the airway within hours of symptoms developing

150
Q

How might epiglottitis present?

A
  • Patient presenting with a sore throat and stridor
  • Drooling
  • Tripod position, sat forward with a hand on each knee
  • High fever
  • Difficulty or painful swallowing
  • Muffled voice
  • Scared and quiet child
  • Septic and unwell appearance
151
Q

What investigation should be done for epiglottitis?

A

lateral XR of the neck shows a characteristic “thumb sign” or “thumbprint sign”.

152
Q

When does respiratory failure occur?

A

when there is a failure of gas exchange and/or ventilation, leading to abnormalities in arterial oxygen partial pressure (PaO2) and arterial carbon dioxide partial pressure (PaCO2)

153
Q

What is type 1 respiratory failure?

A

hypoxaemia (PaO2 <8 kPa / 60mmHg) with normocapnia (PaCO2 <6.0 kPa / 45mmHg)

V/Q mismatch

154
Q

What is type 2 respiratory failure?

A

hypoxaemia (PaO2 <8 kPa / 60mmHg) with hypercapnia (PaCO2 >6.0 kPa / 45mmHg)

hypoventilation

155
Q

What happens in type 1 resp failure?

A
  • usually occurs due to ventilation/perfusion (V/Q) mismatch
  • PaO2 falls, and PaCO2 rises.
  • The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shapes of the CO2 and O2 dissociation curves.
156
Q

What can cause type 1 resp failure?

A
  • Reduced ventilation and normal perfusion (e.g. pneumonia, pulmonary oedema, bronchoconstriction)
  • Normal ventilation and reduced perfusion (e.g. PE)
157
Q

What can cause type 2 resp failure?

A

Exacerbation of COPD
Opiate overdose/sedation
Rib fractures
Guillain-Barré syndrome

hypoventilation

158
Q

What happens in type 2 resp failure?

A
  • alveolar hypoventilation prevents patients from being able to adequately oxygenate and eliminate CO2 from their blood.
  • This leads to PaO2 falling and PaCO2 rising
159
Q

What investigations should be done for resp failure?

A

Pulse oximetry
ABG

160
Q

What is the first line treatment for resp failure?

A

supplemental oxygen

161
Q

What is pharyngitis?

A
  • pharyngeal inflammation
  • characterised by the rapid onset of sore throat
162
Q

What normally causes pharyngitis?

A

group A strep
viral causes like EBV

Ix: rapid antigen test for group A Streptococcus (GAS)

163
Q

What is croup?

A

upper respiratory tract infection causing oedema in the larynx
typically affects kids age 6 months - 2 years

164
Q

What is the common cause of croup?

A

parainfluenza virus

165
Q

How does croup present?

A

Increased work of breathing
“Barking” cough, occurring in clusters of coughing episodes
Hoarse voice
Stridor
Low grade fever

166
Q

How is croup managed?

A

first line oral dexamethasone

167
Q

What is whooping cough?

A
  • an upper respiratory tract infection caused by Bordetella pertussis (a gram negative bacteria).
  • called “whooping cough”, because the coughing fits are so severe that the child is unable to take in any air between coughs and subsequently makes a loud whooping sound as they forcefully suck in air after the coughing finishes
168
Q

How is whooping cough treated?

A
  • pertussis is notifiable disease
  • supportive care
  • Macrolide abx (azithromycin, erythromycin and clarithromycin) can be beneficial in the early stages (within the first 21 days)
169
Q

How is whooping cough diagnosed?

A
  • A nasopharyngeal or nasal swab with PCR testing or bacterial culture (within 2 to 3 weeks of the onset of symptoms)
  • if sx more than 2 weeks patients: anti-pertussis toxin IgG
170
Q

What is hypersensitivity pneumonitis?

A

inflammation of the alveoli and distal bronchioles caused by an immune response to inhaled allergens
non-IgE mediated immunological inflammation
type 3 and 4 hypersensitivity

171
Q

What can cause hypersensitivity pneumonitis?

A

bacteria e.g. actinomycetes (farmer’s lung)
inhalation of non-human protein
- animal proteins, e.g. avian
mould in workplace
chemical occupational exposure

occupational exposure

172
Q

How does hypersensitivity pneumonitis present?

A

Dyspnoea
Cough
Mid inspiratory squeaks
Systemic symptoms
Chest tightness
wheezing

173
Q

What are some risk factors for hypersensitivity pneumonitis?

A

smoking
viral infection
exposure
- avian protein antigen
- mould antigen
- bacterial antigen
- diisocyanate (e.g., epoxy resin)
- acid anhydride antigen (e.g., paint refinisher)
- metalworking fluid
drugs: nitrofurantoin, methotrexate, roxithromycin, and rituximab

174
Q

What would imaging show for hypersensitivity pneumonitis?

A

CXR: infiltrates, nodular or patchy; fibrosis
CT chest: ground-glass shadowing/attenuation, poorly defined micronodules, mosaic attenuation, centrilobular nodules, basal sparing

175
Q

What investigations should be done for hypersensitivity pneumonitis?

A

CXR
CT chest
serum antigen-specific IgG or IgA: positive
pulmonary function test: restrictive
diffusing lung capacity of carbon monoxide: decreased

176
Q

What would bronchoalveolar lavage show in hypersensitivity pneumonitis?

A

positive antibody + lymphocytosis (elevated CD8+ cells)

177
Q

How is hypersensitivity pneumonitis managed?

A

avoidance of causative agent
consider corticosteroid: prednisolone

178
Q

What are the possible complications of hypersensitivity pneumonitis?

A

progressive deterioration in lung function
hypoxaemia

main point is to avoid trigger

179
Q

What is cryptogenic organising pneumonia? and how does it present

aka: bronchiolitis obliterans

A

focal area of inflammation of the lung tissue
presents: hortness of breath, cough, fever and lethargy, inspiratory crackles

180
Q

How is cryptogenic organising pneumonia diagnosed and treated?

A

Ix: CXR and lung biopsy
Mx: corticosteroids

181
Q

What is TB?

A

an infectious disease caused by Mycobacterium tuberculosis

182
Q

How is Mycobacterium tuberculosis microbiologically classified?

A

Acid fast bacilli
Stained using Ziehl-Neelsen
appear as red stain on a blue background

183
Q

How does TB spread?

A

infection by inhalation of aerosolised particles (droplet nuclei)

184
Q

What is latent TB?

A

immune system encapsulates the bacteria and stops the progression of the disease
no symptoms
not infectious

185
Q

What is primary active TB?

A

active infection after exposure

186
Q

What is secondary active TB?

A

reactivation of latent TB to active infection
usually due to immunosuppression

187
Q

What is the pathophysiology of TB?

A

TB phagocytosed by alveolar macrophages but survive forming caseous granulomas
Granuloma contains and prevents spread of TB
Immunosuppression leads to reactivation, e.g. immunocompromised or steroid use

188
Q

What is a cold abscess?

A

firm, painless abscess caused by TB
usually in the neck.
do not have the inflammation, redness and pain

189
Q

Where can extrapulmonary TB affect?

A

lymph nodes
CNS
bones/joints
GU tract
abdomen
pericardium

mostly in lungs for oxygen

190
Q

What are the risk factors for TB?

A

exposure to infection
birth in an endemic country: Asia, Latin America, and Africa
HIV infection
immunosuppressive medicines: steroids, TNF-alpha antagonists
silicosis
apical fibrosis

191
Q

What are the signs and symptoms of TB?

A

Fever
Malaise
pleuritic chest pain
cough longer than 2-3 weeks
night sweats
weight loss
haemoptysis
psychological symptoms
clubbing
erythema nodosum
lymphadenopathy
Spinal pain in spinal tuberculosis (also known as Pott’s disease of the spine)

192
Q

What is miliary TB?

A

a severe and disseminated form of tuberculosis (TB)

193
Q

What does a CXR show for TB?

A

Primary TB: patchy consolidation, pleural effusions and hilar lymphadenopathy.
Reactivated TB: patchy or nodular consolidation with cavitation (gas-filled spaces), typically in the upper zones.
Disseminated miliary tuberculosis: millet seeds uniformly distributed across the lung fields.

194
Q

What investigations should be done for TB?

A

CXR: upper lobe infiltrates
Sputum cultures (3): positive for M.tb
Sputum acid-fast bacilli smear: positive
nucleic acid amplification testing: positive for M.tb
FBC and electrolytes

195
Q

What does the Mantoux test test for?

A

an immune response to tuberculosis caused by previous infection, latent TB or active TB
injects tuberculin into the intradermal space on the forearm

196
Q

How is latent TB managed?

A

Latent tuberculosis is treated with either:
* Isoniazid and rifampicin for 3 months
* Isoniazid for 6 months
* Pyridoxine prescribed with isoniazid to avoid B6 deficiency

197
Q

How is active TB managed?

A

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

While infectious, patients should remain isolated

198
Q

What should be prescribed with isoniazid?

A

B6 (Pyridoxine)

199
Q

What are the side effects of the TB treatments?

A

Rifampicin: red/orange discolouration of secretions, such as urine and tears. It is a potent inducer of the cytochrome P450 enzymes and reduces the effects of drugs metabolised by this system, such as the combined contraceptive pill.
Isoniazid: peripheral neuropathy. Pyridoxine (vitamin B6) is co-prescribed to reduce the risk.
Pyrazinamide: hyperuricaemia (high uric acid levels), resulting in gout and kidney stones.
Ethambutol: colour blindness and reduced visual acuity.

RIP are all hepatotoxic

200
Q

What should be checked before starting TB therapy?

A

Liver function

201
Q

What is pneumonia?

A

infection of the lung tissue, causing inflammation in the alveolar space

a lower resp tract infection

202
Q

What are the lower resp tract infections?

A

Pneumonia
Acute bronchitis

203
Q

What are the different classifications of pneumonia?

A

Community-acquired pneumonia (CAP) develops in the community
Hospital-acquired pneumonia (HAP) develops after more than 48 hours in a hospital
Ventilator-acquired pneumonia (VAP) develops in intubated patients in the intensive care unit

204
Q

What is aspiration pneumonia?

A

infection develops due to the aspiration of food or fluids, usually in patients with impaired swallowing (stroke, dementia)

anaerobic bacteria

205
Q

Who does hospital acquired pneumonia (HAP) tend to affect?

A

more common in patients in ICU, those who have recently had major surgery, and those who have been in hospital for a long time

mortality high as patients often have comorbidities/ critically ill

206
Q

What are the risk factors for HAP?

A

poor infection control/hand hygiene
intubation and mechanical ventilation
multidrug-resistant bacteria
aspiration

207
Q

What are the risk factors for CAP?

A

age >65 years
residence in a healthcare setting
COPD
exposure to cigarette smoke
alcohol abuse
poor oral hygiene
use of acid-reducing drugs: PPIs
contact with children

208
Q

Which bacteria can cause CAP?

A

Streptococcus pneumoniae
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Haemophilus influenzae
Staphylococcus aureus

209
Q

What bacteria can cause HAP?

A

aerobic gram-negative bacilli
- MRSA
- Pseudomonas aeruginosa
- Escherichia coli
- Klebsiella pneumoniae
- Streptococcus pneumoniae (if early onset, less than 5 days in hosp)

210
Q

What is atypical pneumonia?

A

Caused by organisms that cannot be cultured in the normal way or detected using a gram stain.
Treatment with penicillin is ineffective.
They are treated with macrolides (clarithromycin), fluoroquinolones (levofloxacin) and tetracyclines ( doxycycline)

211
Q

What are the 4 ways pathogens can reach the lower resp tract?

A
  • Inhalation
  • Aspiration of oropharyngeal secretions into the trachea, the primary route through which pathogens enter the lower airways
  • Haematogenous spread from a localised infected site (e.g., right-sided endocarditis)
  • Direct extension from adjacent infected foci (e.g. TB)
212
Q

What confirms a diagnosis of HAP?

A

New shadowing on CXR + 2 of:
Fever >38ºC
Leukocytosis or leucopenia
Purulent sputum
Decline in oxygenation

213
Q

What are the symptoms of pneumonia?

A

Fever
Cough
Dyspnoea
Pleuritic chest pain
Mucopurulent sputum
Myalgia
Haemoptysis

214
Q

What score is used to grade severity of CAP?

A

CRB-65 severity score: consider inpatient if above 0
low risk: 0-1
moderate: 2
high: 3-5

215
Q

What investigations should be done for pneumonia?

A

CXR: consolidation (new shadowing)
ABG and pulse oximetry: low O2 sats
U&Es: urea >7 mmol/L
FBC: leukocytosis
CRP: elevated
Sputum culture in HAP

216
Q

What is seen on a CXR for pneumonia?

A

Consolidation (new shadowing)

217
Q

How is CAP managed?

A

Low severity: oral amoxicillin
Moderate: amoxicillin + clarithromycin
Severe: IV amoxicillin/clavulanate + clarithromycin in hospital

218
Q

How is HAP treated?

A

IV broad spectrum Abx
- Mild/moderate: oral amoxicillin/clavulanate
- Severe: IV abx e.g. ceftriaxone or cefuroxime

219
Q

What are the complications of pneumonia?

A

Sepsis
ARDS
Pleural effusion
Empyema
Lung abscess
Death

220
Q

What are the different lung cancers?

A

Small cell (20%)
Non-small cell (80%)
Mesothelioma

221
Q

What is small cell lung cancer and appearance of cells?

A

a malignant epithelial tumour arising from cells lining the lower respiratory tract.

The tumour cells are
- small and densely packed
- scant cytoplasm
- finely granular nuclear chromatin
- absence of nucleoli
- contain neurosecretory granules that release neuroendocrine hormones.

222
Q

What causes lung cancer?

A

approximately 90% of lung cancer is directly attributable to smoking, including virtually all cases of SCLC

223
Q

What is mesothelioma?

A

a lung malignancy affecting the mesothelial cells of the pleura.
strongly linked to asbestos inhalation

prognosis is very poor. Chemotherapy can improve survival, but it is essentially palliative

224
Q

How could lung cancer present in a patient?

A

Persistent cough associated with haemoptysis or weight loss in a smoker older than 50 years of age

225
Q

What are the symptoms of lung cancer?

A

Cough
chest pain
haemoptysis
dyspnoea
weight loss
fatigue

finger clubbing in NSCLC

distant metastasis at presentation common

226
Q

What are the main types of non-small cell lung cancer?

A

adenocarcinoma
squamous cell carcinoma
large cell carcinoma

227
Q

What are the risk factors for lung cancer?

A

cigarette smoking
environmental tobacco exposure
radon gas exposure

228
Q

What could be seen on a CXR in lung cancer?

A

central or peripheral mass
hilar lymphadenopathy
superior mediastinal lymphadenopathy
pleural effusion

229
Q

Where does lung cancer commonly metastasise to?

A

lungs
liver
brain
bone
adrenal glands

230
Q

What investigations should be done for lung cancer?

A

CXR
CT chest, lower neck, abdo
Bronchoscopy
Biopsy

231
Q

What is the treatment for lung cancer?

A

Surgery in NSCLC
chemo and radiotherapy for both

232
Q

What is pneumoconiosis?

A

Lung disease caused by inhalation of mineral
dust

233
Q

What is silicosis?

A

interstitial lung disease caused by breathing in tiny bits of silica, a common mineral found in many types of rock and soil

234
Q

What are some examples of hypersensitivity pneumonitis?

A

Bird-fancier’s lung is a reaction to bird droppings
Farmer’s lung is a reaction to mouldy spores in hay
Mushroom worker’s lung is a reaction to specific mushroom antigens
Malt worker’s lung is a reaction to mould on barley

235
Q
A

Phase 2a (14 decks)

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