Respiratory Flashcards

1
Q

Define the following volumes:

  1. Tidal volume
  2. Inspiratory reserve volume
  3. Expiratory reserve volume
  4. Residual volume
A
  1. TIDAL VOLUME = Amount of air that enters and exits the lung with each normal breath. Normal value = 500mL
  2. INSPIRATORY RESERVE VOLUME = Amount of air that can be inspired with maximal effort after a normal tidal inspiration. Normal value = 3000 mL
  3. EXPIRATORY RESERVE VOLUME = Amount of air that can be expired with maximal effort after a normal tidal expiration. Normal value = 1100 mL
  4. RESIDUAL VOLUME = Amount of air that remains in the lungs after a maximal expiration. Normal value = 1200 mL
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2
Q

Define the following capacities:

  1. Inspiratory capacity
  2. Functional residual capacity
  3. Vital capacity
  4. Total lung capacity
A
  1. INSPIRATORY CAPACITY = Tidal volume + inspiratory reserve volume. Normal value = 3500 mL
  2. FUNCTIONAL RESIDUAL CAPACITY = Residual volume + expiratory reserve volume. Normal value = 2300 mL
  3. VITAL CAPACITY = Tidal volume + inspiratory reserve volume + expiratory reserve volume. Normal value = 4600 mL
  4. TOTAL LUNG CAPACITY = Vital capacity + Residual volume. Normal value = 5800 mL
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3
Q

What muscle are used in inspiration?

What muscles are used in expiration?

A

Inspiratory muscles = diaphragm, external intercostals
Expiratory muscles = with normal quiet breathing elastic recoil is sufficient for expiration, but with heavy breathing extra force can be achieved by contraction of the internal intercostals and rectus abdominis.

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4
Q

What are the accessory muscles of respiration?

A

Scalene muscles

Sternocleidomastoic muscle

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5
Q

The long has a tendency to recoil inwards. What causes this elastic recoil?

A

Elastic recoil is caused by:

  1. ELASTIC FIBERS in the lung. When the lungs expand, the fibers are stretched, but they have a tendency to return to their resting length.
  2. SURFACE TENSION. The water lining the alveoli has surface tension, which leads to their inward collapse.
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6
Q

Explain surface tension and Laplace’s law.

What is surfactant and what effect does it have on surface tension?

A

Surface tension is the force that pulls a liquid’s surface molecules together at an air-fluid interface.
Laplace’s law states that surface tension is greater as the radius of the alveolus decreases - this means that the smaller an alveolus is, the greater the drive to collapse.
Surfactant decreases this surface tension.
In the lungs, the most important surfactant is dipalmitoyl phosphatidylcholine.

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7
Q

Outline the steps of the breathing cycle.

A

INSPIRATION:
1. Brain initiates a respiratory effort.
2. Nerves carry this command to respiratory muscles.
3. Diaphragm and external intercostals contract.
4. Thoracic volume increases due to chest expansion.
5. Intrapleural pressure becomes more negative.
6. Alveolar transmural pressure difference increases.
7. Alveoli expand in response to increased transmural pressure difference.
8. Alveolar pressure falls below the atmostpheric pressure as a result
9. A pressure difference is created that causes air to flow into the alveoli until the alveolar pressure equals the atmospheric pressure.
EXPIRATION:
1. Brain ceases inspiratory command
2. Inspiratory muscles relax
3. Thoracic volume passively decreases due to recoil
4. Intrapleural pressure becomes more positive as a result
5. This decreases the alveolar transmural pressure difference
6. Causes the alveoli to decrease in volume
7. Causes pressure within the alveoli to increase
8. Establishes a pressure difference for airflow that causes air to leave the alveoli until alveolar pressure equals atmospheric pressure

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8
Q

List and explain the roles of the groups in the brainstem that are responsible for the control of breathing.

A

The respiratory centre is composed of several groups of neurons:
1. DORSAL respiratory group (in the NTS of the dorsal medulla) - generates action potentials that cause INSPIRATION.
2 PNEUMOTAXIC centre (in the nucleus parabrachialis of the pons) - controls DURATION OF INSPIRATION. When the signal from this centre is strong, inspiration is short; when the signal is weak, inspiration is longer.
3. VENTRAL respiratory group (in the nucleus ambiguus and nucleus retroambiguus of the medulla) - is inactive during normal respiratory, but causes POWERFUL EXPIRATION.

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9
Q

Explain how the levels of chemicals and gases in the body affect respiration.

A

Excess CO2 or H+ act directly on the respiratory centre, stimulating increased strength of the respiratory commands to respiratory muscles.
Oxygen does not have a significant direct effect, but it acts on peripheral chemoreceptors in the carotid body and aortic body which in turn transmit the signal to the respiratory centre. A decrease in PaO2 stimulates respiration.
The most important factor is CO2. It has a greater effect that O2 and H+.

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10
Q

Describe the structure of haemoglobin.

A

Hb is a tetramer, with 4 monomers that each consist of a heme and a globin. The heme contains an iron atom. In normal adult Hb, there are 2 alpha globin chains and 2 beta globin chains.

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11
Q

What factors shift the oxygen dissociation curve?

In what direction do they shift the curve?

A

The oxygen-dissociation curve describe how strongly oxygen is bound to Hb and how much is is unloaded from the Hb.
The 4 factors that affect this curve are:
1. Temperature
2. pCO2
3. 2,3-diphosphoglycerate
4. pH
An increase in temperature and pCO2 occurs in metabolically active tissues. This causes the curve to shift to the right so that more oxygen is supplied when needed.
Metabolically active tissues also have a lowered pH. When the pH is lowered the curve moves to the right so that more oxygen is supplied. This is known as the Bohr effect.
2,3-DPG is produced as byproduct of glycolysis (occurs in hypoxia, anemia and elevated altitude). Increased 2,3-DPG also shifts the curve to the right. This increases the unloading of oxygen to tissues in hypoxic conditions.

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12
Q

How is CO2 transported in the blood?

A

CO2 is transported from tissues back to the lungs for excretion as:
5% bound to protein
5% dissolved in the blood
90% present as bicarbonate.
For CO2 to be converted into bicarbonate efficiently, carbonic anhydrase is required. This enzyme is present at high concentrations in RBCs.

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13
Q

On general inspection in a respiratory exam, what would you look for?

A
Does the patient look unwell? Distressed?
Obvious cyanosis?
Obvious breathlessnes?
Breathing that is rapid or laboured?
Use of accessory muscles of respiration?
Tripod position?
Pursed lip breathing?
Coughing?
Obvious noise - stridor? wheeze? rattling?
Hoarse voice?
On oxygen? Requiring puffer?
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14
Q

Explain what you would look for in the patients hands/wrists during a respiratory examination.

A
  1. NAILS -
    - Clubbing. 80% of clubbing has a respiratory cause.
    - Nicotine stains
    - Peripheral cyanosis
  2. FINGERS/PALMS
    - Wasting of the small muscles of the hand can occur with an apical lung tumour invading the T1 root
  3. WRISTS
    - Pulse
    - Respiratory rate
    - Hypertrophic pulmonary osteoarthropathy
    - Asterixis (caused by CO2 retention)
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15
Q

What are the respiratory causes of clubbing?

A

Common respiratory causes of clubbing are:

  • Lung cancer
  • Bronchiectasis
  • Lung abscess
  • Empyema
  • Idiopathic pulmonary fibrosis
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16
Q

What would you look for in the face of a patient in a respiratory examination? (6)

A
  1. FACE
    - Plethora of SVC obstruction
    - Red/leathery appearance of a long-term smoker
  2. EYES
    - Conjunctival pallor
    - Horner’s syndrome (pancoast’s tumour)
  3. MOUTH
    - Central cyanosis
    - Signs of URTI: erythema, tonsillar enlargement, pus
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17
Q

Explain the essential parts of examining the neck in a respiratory exam. (4)

A

Inspect for use of accessory muscles.
Assess the position of the trachea.
Feel for a tracheal tug - rest a finger on the trachea during inspiration (a tug causes the finger to move inferiorly)
Palpate cervical and supraclavicular lymph nodes

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18
Q

What would you inspect for in the chest during a respiratory examination? (5)

A
Inspect from the front, back and both sides.
SHAPE
- Barrel shaped
- Pectus carinatum (pigeon chest)
- Pectus excavatum (funnel chest)
- Kyphosis (forward curvature)
- Scoliosis (lateral curvature)
SYMMETRY OF CHEST EXPANSION
SCARS
RADIATION THERAPY SIGNS
- Erythema
- Skin thickening
- Tattoo
PROMINENT VEINS from SVC obstruction
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19
Q

Explain your approach to a frontal CXR.

A
  1. check the DETAILS
    - Patient details: name, DOB, sex
    - Film details: PA, AP, erect, supine, date and time
  2. check the film QUALITY
    PIR - Penetration, Inspiration, Rotation
  3. AIRWAY AND MEDIASTINUM
    - Trachea
    - Widened mediastinum
  4. BREATHING
    - Lungs
    - Pleura
  5. CORONARY AND CIRCULATION
    - Heart
    - Aorta
  6. DIAPHRAGM
    - Costophrenic angle
    - Subdiaphragmatic air
    - Shape: flattened?
    - Height of hemidiaphragms
  7. EXTRAs
    - Tubes, ECG electrodes, pacemaker, defibrillator
  8. SOFT TISSUE and BONE
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20
Q

List the features of pulmonary interstitial oedema on CXR.

A
  1. Pleural effusion
  2. Fluid in fissures
  3. Kerley B lines
  4. Peribronchial cuffing
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21
Q

What are the common causes of pleural effusions? Differentiate the causes of transudates and exudates.

A
Common causes of TRANSUDATES.
- Congestive heart failure
- Hypoalbuminemia
- Cirrhosis
- Nephrotic syndrome
Common cause of EXUDATES.
- Malignancy
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22
Q

What causes an exudate?

What causes a transudate?

A

Exudates are usually caused by inflammation.

Transudates are caused by increased capillary hydrostatic pressure or decreased colloid osmotic pressure.

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23
Q

What does COPD look like on CXR?

A
  • Hyperinflation
  • Flattened diaphragm
  • Hyperlucency with reduced lung markings
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24
Q

What are the normal values during ABG of:

  1. pH
  2. PaCO2
  3. HCO3
  4. Anion gap
A

pH = 7.35-7.45
PaCO2 = 35-45
HCO3 = 22-26
Anion gap = 8-16

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25
Q

During spirometry, what must be present for the obstruction to be considered reversible?

A

The obstruction is reversible if:
Increase of FEV1 of > 12% AND
Increase of > 200mL

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26
Q

What FEV1/FVC ratio defines obstructive airway disease?

A

FEV1/FVC of less than 0.7

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27
Q

How is dyspnoea caused by respiratory disease?
How is dyspnoea caused by cardiovascular disease?
What are other common causes of dyspnoea?

A

Dyspnoea can result from:
RESPIRATORY DISEASE -
1. Any cause of hypercapnia and hypoxia stimulates the respiratory centre in the medulla causes the sensation of air hunger and dyspnoea
2. Disease that affects the respiratory muscles increases the work of breathing and causes the sensation of dyspnoea.
CARDIOVASCULAR DISEASE -
1. Decreased cardiac output (as with CHF) causes a build-up of blood behind the lungs and this increases the pulmonary venous pressure. Increased pressure stimulates receptors in the pulmonary vessels, which produces the sensation of dypsnoea.
OTHER -
1. Anaemia
2. Deconditioning

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28
Q

List 6 respiratory DDX for dyspnoea.

A
Upper airway obstruction - 
1. Foreign object
2. Angioedema
3. Anaphylaxis
4. Infection - epiglottitis
5. Airway trauma
6. Airway burns
Lower airway causes - 
1. Pulmonary embolism
2. COPD - severe COPD or COPD exacerbation
3. Asthma
4. Infection - pneumonia
5. ARDS
6. Pneumothorax
7. Pleural effusion
8. Lung cancer
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29
Q

Give DDX for dyspnoea other than respiratory causes.

Consider - cardiac (give at least 2), neurologic (at least 2), toxins (1), metabolic (1) and other (at least 3).

A
CARDIAC
- Acute coronary syndrome
- Acute decompensated CHF
- Flash pulmonary oedema
- Valvular dysfunction
NEUROLOGICAL
- Guillain-Barre syndrome
- Myasthenia gravis
- Multiple sclerosis
- Motor neuron disease
METABOLIC/TOXINS
- DKA
- Poisons - CO, aspirin
OTHER
- Anaemia
- Hypervention
- Anxiety
- Obesity
- Deconditioning
- Pregnancy
- Sepsis
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30
Q

List investigations that you would consider ordering in a patient presenting with dyspnoea. Also give the disease/s that you are checking for.

A

FBC (anaemia, infection)
Spirometry (reversibility, obstructive vs restrictive disease)
Pulse oximetry (respiratory disease affecting oxygen saturations)
CXR, Chest CT (respiratory disease)
CTPA, V/Q (Pulmonary embolism)
D-Dimer (PE)
Echocardiogram (cardiac causes)
ECG (cardiac causes)
BNP (congestive heart failure)
DLCO (ability of gas to diffuse from lungs into blood)
Venous or arterial blood gas (respiratory causes, acid-base imbalances)

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31
Q

Give your diagnosis of a cough according to the following time course:

  1. Acute cough of < 3 weeks
  2. Subacute cough of 3-8 weeks
  3. Chronic cough of > 8 weeks
A
  1. Common causes of acute cough are:
    - Infection: URTI, pneumonia, COPD exacerbation
    - Asthma exacerbation
    - Aspiration
  2. Common causes of subacute cough are:
    - Post-URTI
  3. Common causes of chronic cough are:
    - Chronic infection - e.g. TB
    - Lung cancer
    - GORD
    - Medications - e.g ACE-inhibitor
    - Congestive heart failure
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32
Q

Give your DDX for haemoptysis. (4)

A

Acute bronchitis
Bronchiectasis
Lung cancer - primary or metastatic
Lung infections

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33
Q

Define stridor.

A

Stridor is an abnormal, high-pitched sound produced by turbulent airflow through a partially obstructed airway at the level of the supraglottis, glottis, subglottis or trachea. It is usually inspiratory, but can also be expiratory (or both).

34
Q

At what point in the breathing cycle does stridor usually occur?

A

Stridor is usually inspiratory.

It can also occur during expiration, or be present through both inspiration and expiration.

35
Q

Give 4 common causes of acute stridor.

Give 3 common causes of chronic stridor.

A
Acute stridor can be caused by:
Croup
Aspiration of a foreign body
Anaphylaxis
Abscess - e.g. retropharyngeal abscess
Epiglottitis
Airway burns
Chronic stridor can be caused by:
Laryngomalacia or tracheomalacia (these structures become floppy and have a reduced ability to maintain patency of the airway lumen)
Vocal cord dysfunction/paralysis
Stenosis of the larynx/trachea
Compression of the airway by a goiter or tumour
36
Q

Define a wheeze.

A

A wheeze is a musical sound heard during chest auscultation that is produced by oscillation of opposing walls of a narrowed proximal conducting airway. It can occur during expiration or inspiration.

37
Q

What is the most common cause of wheeze?

A

Asthma

38
Q

List 4 common obstructive airway diseases.

A

Emphysema
Chronic bronchitis
Asthma
Bronchiectasis

39
Q

Define chronic bronchitis.

A

Chronic bronchitis is defined by the production of sputum on most days for at least 3 months in at least 2 consecutive years.

40
Q

Give risk factors for COPD.

A
  1. Smoking (most important factor!)
  2. Air pollution, both indoor (fires in enclosed spaces) and outdoor
  3. Occupational exposure (dusts, vapours)
  4. Genetic factors (alpha-1-antitrypsin deficiency)
  5. Increasing age
  6. Recurrent respiratory infections
41
Q

Explain the pathogenesis of COPD.

A

Factors involved in the pathogenesis of COPD are:
1. ENHANCED INFLAMMATORY RESPONSE.
In response to inhalation of noxious particles/gases, the lungs have an inflammatory response which is normal and protective. However, in patients who develop COPD this response is increased. As a result of this inflammatory response, there is:
- Increased production of sputum, changes to sputum quality and dysfunction of the mucociliary apparatus.
- Airway wall thickening, with narrowing of the lumen and obstruction
- Parenchymal destruction
2. IMBALANCE IN OXIDANT/ANTI-OXIDANT LEVELS
Smoking and inflammation increase the production of oxidants, causing damage to the lungs.
3. IMBALANCE IN PROTEASE/ANTI-PROTEASE LEVELS
Alpha-1-antitrypsin inhibits serine proteases. A deficiency results in unrestrained proteolytic damage to the lung tissue. Cigarette smoking can inactivate any remaining functional alpha-1-antitrypsin and worsen this.

42
Q

Describe the gross pathology of emphysema.

A

Gross pathology of emphysema:
- Irreversible enlargement of distal airspaces (distal to terminal bronchioles)
- Destruction of airspace walls
This can be centriacinar (proximal part of acini is affected) or panacinar (entire acini is affected).

43
Q

Describe the pathology of chronic bronchitis.

A
  • Hyperplasia of mucus-secreting glands in trachea and bronchi
  • Narrowing of bronchioles caused by mucus plugging
  • With inflammation and fibrosis
44
Q
Explain the pathophysiology of COPD.
Discuss - 
1. Decrease in maximal expiratory flow
2. V/Q mismatch
3. Respiratory muscles
A

The characteristic problem in COPD is a DECREASE IN MAXIMAL EXPIRATORY FLOW.
This is the result of:
1. Increase in airway resistance - from: narrowing due to airway remodelling and exudates blocking the airway
2. Loss of elastic recoil due to destruction of the alveolar walls
The obstruction causes TRAPPING OF AIR DURING EXPIRATION which causes HYPERINFLATION.
In COPD there is also V/Q MISMATCH due to destruction of alveolar walls. This IMPAIRS GAS EXCHANGE.
Normally, exhalation is passive. In COPD it becomes an active process because of reduced elastic recoil. However, in COPD the overinflated lungs mean that respiratory muscles are less able to generate force as the diaphragm is flattened.

45
Q

Give 4 complications of COPD.

A

Repiratory failure
Polycythemia
Pulmonary hypertension
Cor pulmonale

46
Q

What symptoms might a person with COPD complain of?

A

Dyspnoea on exertion
Chest tightness
Chronic cough
Sputum production

47
Q

What is a pink puffer?

What is a blue bloater?

A

Pink puffers often have emphysema. They over-ventilate to maintain well-oxygenated and appear pink as a result.
Blue bloaters often have chronic bronchitis. They do not over-ventilate and so become hypoxic, which gives them a blue tinge.

48
Q

What features might you notice on general inspection of a patient with COPD?

A
Increased respiratory rate
Use of accessory muscles of respiration - SCMs, scalenes
Prolonged expiratory phase
Pursed lip breathing
Tripod positioning
Drowsiness due to CO2 retention
49
Q

During a respiratory examination of a patient with COPD, what might you notice when:

  1. Inspecting the chest
  2. Palpating the chest
  3. Percussing the chest
  4. Auscultating the chest
A
  1. Inspection - barrel shaped chest with increased AP diameter, horizontal ribs, wide subcostal angle
  2. Palpation - decreased chest expansion due to hyperinflation
  3. Percussion - hyper-resonant percussion note
  4. Auscultation - wheeze, reduced breath sounds
50
Q

In a patient with COPD, after examination of the respiratory system, what else should you examine?

A

Cardiovascular examination - for signs that the right heart is being affected -
- Right heart failure
- Right ventricular hypertrophy/dysfunction - heave, gallop rhythm
Abdominal examination - for:
- Liver - (1) palpable below costal margin due to lung hyperinflation; (2) tender and pulsatile due to R heart dysfunction.

51
Q

COPD is a systemic disease. What are the systemic effects? What is thought to be the cause?

A

Inflammation is thought to spill over from the lungs and have systemic effects. These are:

  • Cachexia
  • Myopathy and sarcopenia
  • Vasculopathy - increased coronary and cerebrovascular disease
  • Osteoporosis
  • Possibly depression
52
Q

What investigations would you order in a patient with COPD? Give 5 that would be useful and explain why.

A
  • Spirometry (confirms obstructive disease)
  • Arterial blood gas (confirm the degree of hypoxia and hypercapnia, presence and type of respiratory failure)
  • FBC (polycythemia can develop)
  • Alpha-1-antitrypsin deficiency screening (if the patient is young/non-smoker/has family history, can be useful to determine if there is a genetic cause)
  • Chest x-ray of chest CT (confirm diagnosis, exclude other pathology)
  • ECG (may show signs of cor pulmonale)
53
Q

How would you manage COPD? Hint: COPDX

A

C - Confirm diagnosis and assess severity.
- Spirometry
O - Optimise function
- Non-pharmacological:
Smoking cessation
Pulmonary rehabilitation
Physical activity
- Pharmacological:
Follow a stepwise approach until adequate control is achieved. Start with a short acting reliever, usually a B2 agonist. As the disease progresses, add a long-acting B2 agonist (or muscarinic antagonist). Severe disease may require an inhaled corticosteroid.
P - Prevent deterioration
- Smoking cessation - 5A’s at every visit
- Vaccinations - influenza vaccine annually and pneumococcal vaccine at diagnosis and then every 5 years
- Long term oxygen therapy when PO2 < 55mmHg (or <60 mmHg if there are signs of hypoxia-induced compromise)
D - Develop support networks and self-management plans
- Support groups
X - Manage eXacerbations
- Early diagnosis and hospitalisation essential
- Give inhaled bronchodilator every 3-4 hours
- Give oral corticosteroids for 5 days and then stop
- If signs of infection give antibiotics
- Give oxygen, but aim for a saturation of 88-92%. Avoid high flow and use nasal prongs at 0.5-2L/min.

54
Q

Define asthma.

A

Asthma is a chronic respiratory disorder with
VARIABLE AIRWAY OBSTRUCTION and
AIRWAY HYPER-RESPONSIVENESS.

55
Q

Give risk factors for the development of asthma.

A
Genetic factors:
- Atopy
- Family history of asthma
Environmental factors:
- Exposure to allergens in childhood
- Respiratory infections - RSV and rhinovirus infections are predictive of asthma development
- Exposure to tobacco smoke
- Exposure to air pollution
56
Q

What causes airway narrowing in asthma? (5 factors)

A

Airway narrowing is the final common pathway that causes symptoms of asthma. This narrowing is caused by:

  • BRONCHOCONSTRICTION: contraction of smooth muscle is caused by neural mechanisms or cytokines.
  • AIRWAY HYPER-RESPONSIVENESS: this constrictor response is exaggerated
  • AIRWAY REMODELLING: over time, structural changes occur - e.g. wall thickening, hyperplasia of mucous glands, inflammation, collagen deposition.
  • AIRWAY OEDEMA: this occurs in the airways due to inflammatory mediators increasing the leakiness of lung microvasculature.
  • MUCOUS HYPERSECRETION: mucous plugs can add to the narrowing and obstruction.
57
Q

On microscopy, what might be seen in the airways of a person with asthma? (7)

A
  • Thickened and oedematous airway mucosa
  • Infiltration with inflammatory cells
  • Hypertrophy of smooth muscle cells
  • Denuded portions of epithelium
  • Secretory gland hyperplasia and mucous hypersecretion
  • Mucous plugging of the airways
  • Proliferation of myofibroblasts with increased collagen deposition and fibrosis
58
Q

What are the classic symptoms of asthma?

A
Wheeze
Cough
Shortness of breath
Chest tightness
These are non-specific, but typically in asthma, these symptoms are:
- Episodic
- Related to characteristic triggers
- Associated with a strong family history of asthma
59
Q

What is pulsus paradoxus?

A

A fall in systolic BP during inspiration that is > 12 mmHg

60
Q

What clinical features would you notice in a patient with severe asthma?

A
Laboured respiration
Tachycardia, with HR of 110 or greater
Tachypnoea with RR of 25 or greater
Use of tripod position
Use of accessory muscles of respiration
Pulsus paradoxus
Unable to complete a sentence in 1 breath.
61
Q

Explain the following tests. Why are they useful in the investigation of asthma?

  1. Spirometry
  2. Airway challenge testing
  3. Peak expiratory flow
  4. Exhaled NO
  5. FBC with differential
  6. Allergy testing - total serum IgE, RAST testing (i.e. specific IgE), skin prick testing
A
  1. Spirometry - in asthma, shows obstruction (FEV1/FVC of <0.7) and reversibility (give bronchodilator and repeat the test after 10-15min. Reversibility is present if the FEV1 increases by at least 12% and at least 200mL).
  2. Airway challenge testing - methacholine can be given to stimulate bronchoconstriction. In asthma, hyper-responsivness can be demonstrated by an increased response.
  3. Peak expiratory flow - this is a forceful expiration that is measured in patients with a known diagnosis of asthma to monitor the disease.
  4. Exhaled NO - Nitric oxide on the patient’s breath indicates increased eosinophils in the airway.
  5. FBC with differential - can show elevated eosinophils, which would correlate with asthma
  6. Allergy tests - can be used to confirm an asthma trigger
62
Q

Discuss the long-term treatment of asthma.

A

Successful long-term asthma management involves:
1. Routine monitoring - patient should be followed-up regularly (at least every 6 months).
2. Avoidance of triggers
3. Medications - the medications used depend on the severity of the asthma:
- Intermittent = short-acting B2 agonist when required
- Mild and persistent = SABA plus preventer (usually low dose inhaled corticosteroid)
- Moderate and persistent = longer acting B2 agonist plus preventer (low dose inhaled corticosteroid)
- Severe and persistent = possibilities include:
Inhaled glucorticoid + long-acting B2 agonist
PLUS possibly leukotriene modifier
PLUS possibly oral glucocorticoid
PLUS possibly anti-IgE therapy
PLUS possibly anti-IL5 therapy
4. Patient education

63
Q

Define restrictive lung disease.

A

Restrictive lung disease is characterised by:

  1. DECREASED TOTAL LUNG CAPACITY
  2. PRESERVED EXPIRATORY FLOW
  3. NORMAL FEV1/FVC RATIO
64
Q

What are the two main groups of restrictive lung disease?

A
  1. Interstitial lung diseases

2. Extra-pulmonary disease involving the chest wall and respiratory muscles

65
Q

What is bronchiectasis?

A

Permanent dilation of the bronchi caused by destruction of the elastic and muscular components in the bronchial wall, which is usually due to severe and/or recurrent infections.

66
Q

Describe the pathogenesis of bronchiectasis.

A

Bronchiectasis develops when there is an infectious insult in the presence of impaired drainage, airway obstruction or defective host defenses. There is an immune response that causes inflammation, which damage the walls of the airways (via ROS, proteases and cytokines). The walls are destroyed, which causes permanent abnormal dilation.

67
Q

What is the usual presentation of bronchiectasis?

A

Cough with daily production of sputum that is mucopurulent and lasts for months to years.

68
Q

What is atelectasis?

A

Atelectasis is loss of lung volume caused by collapse of lung tissue.

69
Q

What causes atelectasis?

A

Atelectasis can be caused by obstructive and non-obstructive causes.
Obstructive atelectasis occurs when there is a blockage of the airway. Air distal to the blockage is absorbed into the capillaries so that these regions become gasless and collapse.
Non-Obstructive atelectasis is less common, but can occur for example with:
- Loss of contact between parietal and visceral pleura - e.g. pneumothorax, pleural effusion
- Loss of surfactant
- Replacement of space by a tumour

70
Q

In what setting does atelectasis most commonly occur?

A

Post-operatively

71
Q

What are the symptoms and signs of atelectasis?

A
Symptoms:
- Dyspnoea
- Chest pain
Signs:
- Early postoperative fever
- Tracheal deviation towards the affected side
- Reduced chest expansion
- Dullness to percussion
- Diminished or absent breath sounds
- If severe: respiratory distress, hypotension, tachycardia, tachypnoea, shock
72
Q

List 4 potential complications of atelectasis?

A

Pneumonia
Sepsis and septic shock
Bronchiectasis
Hypoxemia and respiratory failure

73
Q

Give risk factors for community-acquired bacterial pneumonia.

A

Increased age
Chronic respiratory disease - especially COPD
Immunocompromise (including DM)
Malnutrition
Viral respiratory tract infection
Impaired protection of the airway - e.g. decreased LOC, impaired swallowing after stroke, oesophageal dysmotility
Smoking
Alcohol misuse
Crowded living conditions
Instrumentation of the respiratory tract - e.g. intubation, bronchoscopy

74
Q

What is the most common pathogen that causes bacterial community-acquired pneumonia?

A

Streptococcus pneumoniae

75
Q

List 3 pathogens that commonly cause community-acquired pneumonia in each of the following categories:

  1. Typical bacterial causes
  2. Atypical bacterial causes
  3. Viral causes
A
  1. Typical -
    - Streptococcus pneumoniae
    - Haemophilus influenzae
    - Staphylococcus aureus
  2. Atypical -
    - Legionella spp.
    - Mycoplasma pneumoniae
    - Chlamydia pneumoniae
  3. Viral -
    - Influenzae
    - Rhinovirus
    - Coronavirus
76
Q

List the 4 stages of bacterial pneumonia. Briefly explain each stage.

A
  1. CONGESTION - the lung is heavy, boggy and red due to vascular engorgement. There is intra-alveolar fluid with numerous bacteria and a few neutrophils.
  2. RED HEPATIZATION - the lung appears red, firm and airless (like a liver). The area is filled with exudate as neutrophils, RBCs and fibrin fill the alveoli.
  3. GREY HEPATIZATION - the lung appears grey. The exudate persists but the RBCs break down.
  4. RESOLUTION - the lung returns to a normal appearance as the exudate is broken down and debris reabsorbed, phagocytosed, expectorated or organised.
77
Q

What are the common symptoms of pneumonia?

A

Cough, with or without sputum
Pleuritic chest pain
Dyspnoea
Patients also frequently have GI and systemic symptoms:
GIT - nausea, vomiting, anorexia
Systemic - fever, chills, fatigue, malaise, mental status changes

78
Q

What are the common signs of pneumonia?

A
Tachypnoea
Tachycardia
Reduced chest expansion on the affected side
Dullness to percussion
Bronchial breath sounds
Wheeze
Crackles (coarse)
Increased vocal resonance
79
Q

What investigations would you order in a patient you suspected of having community acquired pneumonia?

A
  1. Chest x-ray
  2. Blood culture
  3. Sputum gram stain, culture and sensitivity
  4. Urinary antigen test for S pneumoniae
  5. FBC
  6. EUC (urea is part of CURB65)
  7. CRP
80
Q

What is CURB65? When is it used? Explain the different parts.

A

CURB65 is used to determine the need to hospitalise a patient with community acquired pneumonia.
C - Confusion present
U - Urea > 7 mmol/L
R - Respiratory rate >30
B - Systolic BP < 90, or diastolic BP < 60
65 - Age over 65 years
Each of these is given 1 point if present.
Patients with a score of 0-1 = outpatient treatment
Patients with a score of 2 = hospitalize
Patients with a score of 3+ = ICU admission

81
Q

What is SMARTCOP? When is it used? Explain the different parts.

A
SMARTCOP is used to determine the severity of pneumonia. 
S - Systolic BP < 90
M - Multi-lobar involvement on CXR
A - Albumin < 35 g/L
R - Respiratory rate of >25 
T - Tachycardia >125bpm
C - Confusion
O - Oxygenation low - i.e. saturation of <92% or PaO2 of <70 mmHg
P - pH of <7.35 (i.e. acidosis)
82
Q

List 5 complications of community acquired pneumonia.

A

Possible complications of CAP are:

  • Lung abscess formation
  • Empyema
  • Bronchiectasis
  • Pleural effusion
  • Sepsis, septic shock
  • Respiratory failure
  • Death