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PBLs > Week 7 - Respiratory > Flashcards

Week 7 - Respiratory Flashcards

1
Q

what are the indications for O2 therapy?

A
  • Hypoxaemia – oxygen does not treat the underlying cause of hypoxaemia, you must take a systematic approach to identify the cause!
    • Exacerbation of longstanding lung disease e.g. COPD, cystic fibrosis, fibrosis
    • Severe kyphosis
    • Respiratory muscle weakness
      Overdoes of drugs causing respiratory depression (opiates, benzodiazepines)
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2
Q

what is the criteria for LTOT?

A
  • pO2 <7.3kPa on ABG, or <8.0kPa with complications (pulmonary hypertension, polycythaemia, peripheral oedema)
    • Non-smoking due to explosion risk
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3
Q

what are the different colours of venturi mask and what O2 do they give?

A

Blue: 2-4L/min, 24% FiO2
White: 4-6L/min, 28% FiO2
Orange: 31% FiO2
Yellow: 8-10L/min, 35% FiO2
Red: 10-12L/min, 40% FiO2
Green: 12-15L/min, 60% FiO2

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4
Q

what are the red flags for lung cancer?

A
  • Haemoptysis (coughing up blood) / rust coloured sputum
    • Finger clubbing
    • Recurrent pneumonia
    • Weight loss
      Lymphadenopathy – often supraclavicular nodes are the first to be found on examination
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5
Q

when should patients be referred on 2ww for lung cancer?

A

○ Have chest X-ray findings that suggest lung cancer, or
Are aged 40 years and over with unexplained haemoptysis.

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6
Q

when should an urgent 2ww CXR be given for suspected lung cancer?

A

people aged 40 years and over if they have two or more of the following unexplained symptoms, or if they have ever smoked and have one or more of the following unexplained symptoms:
§ Cough.
§ Fatigue.
§ Shortness of breath.
§ Chest pain.
§ Weight loss.
§ Appetite loss.

  • Consider an urgent chest X-ray (to be performed within 2 weeks) to assess for lung cancer in people aged 40 years and over with any of the following:
    □ Persistent or recurrent chest infection.
    □ Finger clubbing.
    □ Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy.
    □ Chest signs consistent with lung cancer.
    Thrombocytosis.
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7
Q

what non-medication management is given in COPD?

A

smoking cessation
pneumococcal and annual influenza vaccine
pulmonary rehab

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8
Q

what is the long term medication management for COPD?

A
  1. SABA e.g. salbutamol/SAMA e.g. ipratropium bromide

2a. no asthmatic/steroid responsive feature = combined LABA + LAMA e.g. anoror elipta
2b. if they have asthmatic/steroid responsive features = combined LABA + ICS e.g. fostair/symbicort

  1. if steps 2a/b dont work then can step up to LABA+LAMA+ICS e.g. trimbo/trelegy
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9
Q

what is carbocisteine?

A

oral mucolytic therapy to break down sputum

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10
Q

what treatment is given in COPD exacerbation if patient is well enough to stay home?

A
  • Prednisolone 30mg once daily for 7-14 days (steroid)
    • Regular inhalers or home nebulisers
      Antibiotics if there is evidence of infection
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11
Q

what treatment is given a COPD exacerbation when patient comes to 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

Options in severe cases not responding to first line treatment:

* IV aminophylline
* Non-invasive ventilation (NIV)
* Intubation and ventilation with admission to intensive care
* Doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate
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12
Q

what is a SABA and give examples?

A

short acting beta 2 agonist = bronchodilator
salbutamol or terbutaline

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13
Q

what is a SAMA and give examples?

A

short acting antimuscarinics
ipratropium bromide

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14
Q

what is a LABA and give examples?

A

long acting beta agonist
salmeterol or formoterol

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15
Q

what is a LAMA and give examples?

A

long acting antimuscarinics
tiotropium

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16
Q

what are the side effects of SABAs?

A

Fine tremor
Tachycardia (arrhythmias)
Headache
Palpitations
Hypokalaemia

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17
Q

what are the side effects of SAMAs?

A

Arrhythmias
Constipation
Cough
Dizziness
Dry mouth
Headache
Nausea
Gastrointestinal motility disorder

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18
Q

what are the side effects of LABAs?

A

Muscle cramps
Dizziness
Nausea
Tremor
Tachycardia (arrhythmias)
Headache
Palpitations
Hypokalaemia

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19
Q

what are the side effects of LAMAs?

A

Dry mouth
Difficulties in passing urine in men
Arrhythmias
Constipation
Cough
Dizziness
Headache
Nausea

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20
Q

what is a ICS and give examples?

A

inhaled corticosteroids
prednisolone, beclamethasone

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21
Q

what are some side effects of ICSs?

A

oral candidiasis
dysphonia (hoaseness)
pneumonia

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22
Q

what may be shown on a CXR in COPD?

A

enlarged lungs (hyperinflated), air pockets (bullae) or a flattened diaphragm

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23
Q

which imaging best supports the diagnosis of COPD and what does it show?

A

CT scan

Chronic bronchitis
Bronchial wall thickening
Enlarged vessels
Repeated inflammation = scarring with bronchovascular irregularity and fibrosis

Emphysema
Diagnosed by alveolar septal destruction and airspace enlargement
Centrilobular → predominantly in upper lobes
Panacinar → predominantly in lower lobes
Paraseptal → occurs near lung fissures and pleura
Formation of giant bullae = compression of mediastinal structures
Rupture of pleural blebs may produce spontaneous pneumothorax/pneumomediastinum

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24
Q

what is the gold standard for diagnosing COPD?

A

spirometery

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25
Q

what is FVC?

A

forced vital capacity
the total volume of air that the patient can exhale in one breath is measured

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26
Q

what is FEV1?

A

forced expiratory volume

The amount of air that the patient can exhale in the first second is also measured

27
Q

what is seen on spirometery in COPD?

A
  • COPD patients often have narrowing or inflammation of the airways. This hinders how fast air can leave the lungs
  • This leads to a decrease in FEV1
  • If the FEV1 is decreased disproportionately to the FVC, a diagnosis is made for COPD
    To determine if the decrease is disproportionate, the FEV1/FVC ratio is calculate

An FEV1/FVC ratio <0.07 after bronchodilator is typically diagnostic of COPD

28
Q

what is TLC?

A

total lung capacity
volume of air contained in the lung after full inhalation

29
Q

what is RV in spirometery?

A

residual volume
volume of air left in the lung after full exhalation

30
Q

what is FRC in spirometery?

A

functional residual capacity
volume of gas left in the lungs after a tidal breath

31
Q

what is body plethysmography showing when used in diagnosis of COPD?

A

Body plethysmography is the best way to calculate lung volumes for COPD
COPD changes to lung volumes:
* Emphysema destroys lung tissue, leading to loss of elastic recoil. This allows the lungs to be stretched abnormally large volumes, resulting in an increased TLC
* RV can also be increased in COPD when disease progression destroys the elastic tethers that help hold small airways open during exhalation. This leads to premature closing of the airways, which causes abnormal amount of air to be trapped in the lung
* In some patients , there is also inflammation of the small airways, which causes narrowing, further contributing to air trapping and the increase in RV

32
Q

what is DCLO?

A

diffusing capacity of the lungs using CO
This is a measure of how easily carbon monoxide molecules transfer from the alveolar gas to the haemoglobin of the red cells in the pulmonary circulation
To measure → patient inhales a single breath containing a minute amount of CO and holds it for 10 seconds
Breath is then exhaled and the exhaled breath is analysed for CO
The change in the concentration of the CO is then multiplied by the single breath TLC to calculate the DLCO

33
Q

what does DCLO show in COPD?

A
  • The DLCO decreases with increasing severity of disease
    • This is because in emphysema, lung has lost alveoli, resulting in a lower surface area available for diffusion
    • In addition there is a loss of capillary bed, which can also decrease DLCO
    • When DLCO falls below 55% of predicted, the patient should undergo oximetry during exercise to determine if oxygen is required.
34
Q

what is cor pumonale?

A

right sided heart failure caused by respiratory disease.

The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries. This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system

35
Q

what are the main respiratory causes of cor pulmonale?

A
  • COPD is the most common cause
    • Pulmonary Embolism
    • Interstitial Lung Disease
    • Cystic Fibrosis
      Primary Pulmonary Hypertension
36
Q

what are the symptoms of cor pulmonale?

A

often asymptomatic
may show SOB (but this is also seen in the lung condition they usually have)
peripheral oedema
increased breathlessness on exertion
syncope
chest pain

37
Q

what are the clinical signs of cor pulmonale?

A
  • Hypoxia
    • Cyanosis
    • Raised JVP (due to a back-log of blood in the jugular veins)
    • Peripheral oedema
    • Third heart sound
    • Murmurs (e.g. pan-systolic in tricuspid regurgitation)
      Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
38
Q

what is the management of cor pulmonale?

A

treating underlying cause
LTOT often used to help hypoxia indcued vasoconstricition
prognosis is poor

39
Q

what are the stages that lead to cor pulmonale?

A
  1. lung disorder causes poor oxygenation
  2. the hypoxia leads to pulmonary vasoconstricition
  3. this leads to pulmonary hypertention
  4. its then harder for RV to pump against increased pressure
40
Q

what happens to the RV if cor pulmonale is caused by an acute lung disorder?

A

RV dilates

41
Q

what happens to the RV if cor pulmonale is caused by a chronic lung disorder?

A

RV hypertrophies
this also leads to right sided iscahemia as theres an increased demand and conronary arteries are squashed

42
Q

what is used to diagnose cor pulmonale?

A
  • echocardiogram showing evidence of increased pressure in pulmonary arteries in the RV
    • Spirometer can look for chronic lung disease
      Right heart catheterisation (gold standard) to measure the pulmonary pressures
43
Q

what is the gold standard diagnostic test of cor pulmonale?

A

right sided catheterisation to measure pulmonary pressures

44
Q

what is ILD and how is it caused?

A

interstitial lung disease

  1. acute inflammatory response -> disruption of epithelium and endothelium
  2. causes inflammation
  3. if there is a persisitant irratent the lung tissue keeps on undergoing inflammation and apoptosis and phagocytosis
  4. usually a dysregulated healing response as hronic inflammation and fibroblast overactivity leads to scarring and fibrosis that reaches the parenchyma.
  5. fibrotic tissue is unable to expand and becomes stiff .: poor gas exchange
45
Q

what is pneumoconisis?

A

a group of chronic lung diseases caused by exposure to a mineral dust or a metal, the most common ones are asbestosis, silicosis, coal workers pneumoconiosis (black lung) and beryliosos (berylium disease)

46
Q

what is asbestosis?

A

interstitial fibrosis caused by the inflammation that asbestos fibbers trigger.
Following an inhalation of asbestos, fibres are distributed in the lungs, and macrophages are recruited to clear them, though asbestos is notoriously difficult to digest.
The persistence of these fibres initiates immune responses that recruit fibroblasts that deposit collagen in the interstitial and surrounding tissues.

47
Q

what are some causes of respiratory acidosis?

A

inadequate alveolar ventilation leading to CO2 retention

Causes: respiratory depression e.g. opiates, asthma, COPD, Guillain-Barre, latrogenic

48
Q

what are some causes of respiratory alkalosis?

A

excessive alveolar ventilation, more CO2 than normal exhaled

Causes: panic attack, pain, hypoxia, PE, pneumothorax, latrogenic

49
Q

what is an anion gap?

A

artificial measure to determine presence of unmeasured anions e.g. albumin
*Formula: Na+ - (Cl- + HCO3-), normal gap: 4-12mmol/L

50
Q

what are some causes of metabolic acidosis?

A

increased acid production/acid ingestion OR decreased acid excretion/increased rate of GI and renal HCO3- loss

Causes of high anion gap (due to increased production/ingestion or reduced excretion of H+ by the kidneys: diabetic ketoacidosis. Lactic acidosis, aspirin overdose, renal failure

Causes of normal anion gap (due to loss of HCO3-, which is replaced by Cl in plasma: GI loss of HCO3-, renal tubular disease, Addison’s disease

51
Q

what are some causes of metabolic alkalosis?

A

decreased H+ conc. leading to increased bicarbonate

Causes: GI loss of H+ ions e.g. vomiting, diarrhoea, renal loss of H+ ions e.g. loop and thiazide diuretics, heart failure, cirrhosis, latrogenic

52
Q

what are some causes of mixed respiratory and metabolic acidosis?

A

decreased pH, increase CO2, decreased HCO3-
○ Causes: cardiac arrest, multi-organ failure

53
Q

what are some causes of mixed respiratory and metabolic alkalosis?

A

decreased pH, decreased CO2, increased HCO3-
Causes: liver cirrhosis in addition to diuretic use, hyperemesis gravidarum, excessive ventilation in COPD

54
Q

what are the main types of lung changes that occur with smoking?

A

narrowing and remodelling of the airways
* increased number of goblet cells
* enlargement of mucus-secreting glands of the central airways,
* alveolar loss
vascular bed changes leading to pulmonary hypertension.

55
Q

what effect does smoking have on cilia?

A
  • Toxicants in tobacco smoke paralyse the cilia and eventually destroy them, removing an important protection in the respiratory system.
    • Ciliary dysfunction and increased goblet cell size and number causes the airways to become inflamed and leads to excessive mucus secretion.
    • Excessive mucus secretion impairs ventilation and also makes the lungs more susceptible to infection.
56
Q

what affect does smoking have on the alveoli?

A
  • Smoking also causes the walls of the alveoli to break down and join together, forming larger air spaces than normal.
    Elastin breakdown and subsequent loss of alveolar integrity causes emphysema. The lungs ability to provide the blood with sufficient oxygen to supply the body is thus impaired.
57
Q

what effect does smoking have on the airways?

A
  • Smoking induces airway remodelling which thickens the epithelium, lamina propia, and smooth muscle, causing the airways to become more narrow.
    In addition, reduced elastic recoil, fibrotic changes in lung parenchyma, and also luminal obstruction of airways by secretions, all contribute to increased airway resistance, reducing airflow and causing breathlessness.
58
Q

what is COPD?

A

Chronic Obstructive Pulmonary Disease (COPD) is a chronic respiratory condition characterised by airflow obstruction caused by damage to lung tissue. It is most commonly the result of a combination chronic bronchitis and emphysema as a result of smoking.

59
Q

what are the 2 types of COPD?

A

· Bronchitis – Cough and sputum production on most days for at least 3 months during the last two years.
· Emphysema – Enlarged airspaces distal to the terminal bronchioles, with destruction of the alveolar walls.

60
Q

what is the main result seen on spirometery that indicates COPD?

A

In COPD the FEV1:FVC ratio is <70%.

61
Q

is there reversibility in COPD and asthma?

A

COPD no
asthma yes

62
Q

what is emphysema and how does it occur?

A

Emphysema causes enlarged airspaces distal to the terminal bronchioles, with destruction of the elastin alveolar walls causing decreased elastic recoil.

  1. Loss of elasticity of the alveoli
  2. Inflammation and scarring – reducing the size of the lumen, as well as reducing elasticity
  3. Mucus hypersecretion – reducing the size of the lumen and increasing the distance gasses have to diffuse.
    Emphysematous bullae will often form, which are essentially just large closed off air spaces with trapped air inside them.
63
Q

what is chronic bronchitis and how does it occur?

A

· An enlargement in mucus secreting glands (hypertrophy)
· An increased number of goblet cells (hyperplasia)
· The main cell involved in this reaction are neutrophils.

PBLs (19 decks)

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