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214.201 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is dyspnea?

A

Subjective sensation of uncomfortable breathing

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2
Q

What is severe dyspnea?

A
  • Flaring of the nostrils
  • Use of accessory muscles of respiration
  • Retraction of the intercostal spaces
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3
Q

What is orthopnea?

A

Dyspnea when lying down

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4
Q

What is paroxysmal nocturnal dyspnea?

A

Awaking at night and gasping for air; must sit up or stand up

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5
Q

What is a cough?

A

Protective reflex that helps clear the airways by an explosive expiration

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6
Q

What is a acute cough?

A

Cough that resolves within 2 to 3 weeks

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7
Q

What is a chronic cough?

A

Cough lasting longer than 3 weeks

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8
Q

What is abnormal sputum?

A

Changes in amount, consistency, color, and odour provide information about the progression of disease and the effectiveness of therapy. E.g yellow or green sputum = bacterial infection, pink = blood

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9
Q

What is hemoptysis?

A

Coughing up blood or bloody secretions

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10
Q

What is eupnea?

A

A normal breathing pattern

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11
Q

What are abnormal breathing patterns?

A

Adjustments made by the body to minimise the work of the respiratory muscles

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12
Q

What are Kussmaul respirations (hyperpnea)?

A

Slightly increased ventilatory rate, very large tidal volume, and no
expiratory pause

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13
Q

What is labored breathing?

A

Increased work of breathing

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14
Q

What is restricted breathing?

A

Disorders that stiffen the lungs or chest wall and decrease compliance

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15
Q

What are Cheyne-Stokes respirations?

A

Alternating periods of deep and shallow breathing; apnea lasting 15 to 60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea

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16
Q

What is cyanosis?

A
  • Bluish purple discolouration of the skin and mucous membranes
  • Develops when have five grams of desaturated haemoglobin, regardless of concentration
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17
Q

What is peripheral cyanosis?

A
  • Most often caused by poor circulation

- Best observed in the nail beds

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18
Q

What is central cyanosis?

A
  • Caused by decreased arterial oxygenation (low saturation of oxygen [SO2])
  • Best observed in buccal mucous membranes and lips
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19
Q

What is clubbing?

A
  • Enlargement of tips of fingers and change in angle of the nail bed
  • Amount of soft tissue below nail increases
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20
Q

What is ventilation (V)?

A

Air reaching alveoli

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21
Q

What is perfusion (Q)?

A

Blood reaching alveoli

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22
Q

What is the normal V/Q ratio?

A

0.8-0.9

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23
Q

What does mismatched V/Q cause?

A

Hypoxemia

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24
Q

What does low V/Q ratio cause?

A

Impaired gas exchange,

causing low partial oxygen

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25
Q

What does high V/Q ratio cause?

A

It is caused by pulmonary embolism and result in low partial oxygen

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26
Q

What do pulmonary function tests do?

A
  • Assess the function of the lungs
  • Determine fitness
  • Detect impairment
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27
Q

What do ventilatory function measure?

A

Lung volumes and pressures

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28
Q

What do tests for diffusion of alveolar gases measure?

A

Gases in expired air and in the blood

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29
Q

What is hyercapnia?

A
  • Increased carbon dioxide in the arterial blood
  • Occurs from decreased drive to breathe or an
    inadequate ability to respond to ventilatory stimulation
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30
Q

What is hypoxemia and hypoxia?

A
  • Hypoxemia (blood) versus hypoxia (tissues)

- Ventilation-perfusion abnormalities: Most common cause

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31
Q

What is a spirometer?

A
  • Measures lung volume & capacity
  • Dependent on age, gender, ethnicity & height
  • Measure FEV1 & FVC
32
Q

What is FEV1?

A
  • Forced volume capacity

- Forced expiratory volume in one second

33
Q

What is FVC?

A
  • Forced vital capacity

- Maximum amount of air that can be expired

34
Q

What is normal FEV1/FVC?

A

80%

35
Q

What FEV1/FVC ratio diagnoses COPD?

A

70%

36
Q

What are restrictive defects?

A

Decrease compliance of the lungs or chest wall

37
Q

What are obstructive defects?

A

Block the exchange of air to and from the lungs

38
Q

How do tests for obstructive defects show?

A
  • FEV1 greatly reduced
  • FVC normal or slightly reduced
  • FEV1/FVC below 80%
39
Q

How do tests for restrictive defects show?

A
  • FEV1 slightly reduced
  • FVC reduced proportionally
  • FEV1/FVC normal
40
Q

What are risk factors for COPD?

A
  • Tobacco smoke
  • Pollution
  • Occupational exposure
  • Frequent lower respiratory infections
41
Q

What are risk factors for COPD?

A
  • Tobacco smoke
  • Pollution
  • Occupational exposure
  • Frequent lower respiratory infections
42
Q

What is the main preventative strategy for COPD?

A
  • Tobacco cessation with nicotine replacement
43
Q

What is the pathophysiology of COPD?

A
  • Starts as small airway disease
  • Takes 30 years to progress
  • Irritant causes inflammation of airway epithelium, which infiltrates inflammatory cells & releases cytokines
  • Causes continuous bronchial irritation & inflammation = chronic bronchitis
  • Causes increased protease activity with breakdown of elastin in lung connective tissue = emphysema
  • Accumulation of changes cause airways obstruction, air trapping, & loss of surface area for gas exchange
44
Q

How to diagnose COPD?

A

Spirometry FEV1 less than 80%, FEV1/FVC less than 70%

45
Q

Treatment for COPD?

A

COPD is not curable, but treatment can slow the progress of the disease, control symptoms and improve quality of life for people with the illness

46
Q

How does COPD affect expiration?

A
  • Airway obstruction is worse with expiration

- More force or more time is required to expire a given volume of air; emptying the lungs is slowed.

47
Q

What are the clinical manifestations of COPD?

A
  • Increased work of breathing
  • Ventilation-perfusion mismatching
  • Decreased forced expiratory volume in one second (FEV1)
48
Q

What is emphysema?

A
  • Decrease of elastic recall
  • Destruction of alveolar walls produce dilated air spaces and less surface area for gas exchange
  • Unsupported airways tend to collapse on expiration
  • Obstruction of small
    bronchioles
  • Air trapping (dec. elasticity)
  • Exertional dyspnoea
  • Weight loss
  • Accessory muscle breathing
49
Q

What is air trapping?

A

When bronchial walls collapse during expiration causing air to become trapped

50
Q

How does emphysema affect the lungs?

A
  • Destruction of the alveoli due to elastin breakdown due to imbalance between proteases & anti-protease, oxidative stress & apoptosis of the lung’s structural cells
  • Cause large spaces within lung parenchyma (bullae) & air spaces to pleura (blebs)
51
Q

What are the clinical manifestations of emphysema?

A
  • Dyspnea on exertion
  • Later progresses to marked dyspnea, even at
    rest
  • Little coughing and very little sputum
  • Thin
  • Tachypnea with prolonged expiration; use of accessory muscles for ventilation; pursed lips
  • Barrel chest
  • Tripod position
52
Q

What is chronic bronchitis?

A
  • Recurrent or chronic productive cough for a minimum of 3 months for 2 consecutive years
  • Chronic inflammation, episodic dyspnoea
  • Hypertrophy of secretory bronchial glands cause mucus plugging
  • Cilia are destroyed
  • Bronchoconstriction
  • Increased airflow resistance
  • Increased work of breathing
  • Hypoventilation & CO2 retention causes hypoxemia & hypercapnia
  • Accessory muscle breathing
53
Q

What is the pathophysiology of chronic bronchitis?

A
  • Inflammation of epithelium
  • Enlarged submucosal gland
  • Hyperinflation of alveoli
  • Mucous accumulation & plugging
54
Q

What are the clinical manifestations of chronic bronchitis?

A
  • Decreased exercise tolerance
  • Wheezing and shortness of breath
  • Productive cough becomes copious
  • Polycythemia
  • Decreased FEV1
55
Q

What does Alpha 1-antitrypsin deficiency do?

A
  • Alpha 1-antitrypsin inhibits proteases which protects tissues from neutrophil elastase
  • Deficiency cause neutrophil elastase to breakdown elastin, lower elasticity of lungs and causes complications such as emphysema
  • Neutrophil elastase is secreted by neutrophils during inflammation, it destroys bacteria and host tissue
  • Cigarette smoke can lead to oxidation of a residue of
    Alpha 1-antitrypsin essential for binding elastase
  • 1 in 2500 people
56
Q

What is mild COPD?

A
  • FEV1 60-80%
  • Breathless with moderate exertion
  • Recurrent chest infections
  • Little to no impact on ADL’s
57
Q

What is moderate COPD?

A
  • FEV1 40-59%
  • Increased dyspnea
  • SOB walking on level ground
  • Increased limit on ADL’s
  • Cough & sputum production
58
Q

What is severe COPD?

A
  • FEV1 less than 40%
  • Dyspnea with mild exertion
  • ADL’s severely limited
  • Chronic cough
  • Regular sputum production
59
Q

What are some COPD management ideas that are non-pharmaceutical?

A
  • Pulmonary function tests, ABG’s, chest x-ray, exercise test, dsypnea scales
  • Nutrition interventions since respiratory distress increases calorie needs
  • Oxygen therapy
60
Q

What are some ideas pulmonary rehabilitation for COPD?

A
  • Education
  • Aim to improve lung function & other symptoms
  • Smoking cessation
  • Optimising drug treatment
  • Physiotherapy
  • Recognising worsening symptoms
61
Q

What are medications for COPD?

A
  • Bronchodilators (short or long acting)
    1) Beta-agonists and anticholinergics,
    2) SABA (e.g salbutamol/Ventolin), LABA (eg. Salmeterol), LAAC (eg. tiotropium)
  • Inhaled corticosteroids (ICS)
  • Oral corticosteroids (long term use has side effects)
62
Q

What are COPD exacerbations?

A
  • When pt with COPD experiences sustained (24-48hrs) increase in cough, sputum production, and/or dyspnea
  • Most common causes bacterial or viral infections, annual flu vac, pneumococcal vac
  • Common reason for hospitalisation, and requirement for mechanical ventilation
63
Q

How to manage COPD?

A
  • Drugs- bronchodilators (short and long-acting), Corticosteroids, Antibiotics for infections
  • Pressured Metered Dose Inhalers, Nebulisers, Ventilators
  • Oxygen Therapy or oxygen concentrator
  • Self-Management
64
Q

What are complications of COPD?

A
  • Cor pulmonale

- Right heart failure

65
Q

What is cor pulmonale?

A
  • Secondary to Pulmonary Arterial Hypertension (PAH)
  • Right ventricular enlargement
  • Pulmonary hypertension, creating chronic pressure
    overload in the right ventricle
66
Q

What are clinical manifestations of cor pulmonale?

A
  • Heart appears normal at rest

- With exercise: Decreased cardiac output, chest pain

67
Q

Treatment of cor pulmonale?

A
  • Decrease workload of the right ventricle by lowering
    pulmonary artery pressure
  • Same as for treating PAH
  • Reversal of the underlying lung disease
68
Q

What is the pathophysiology of cor pulmonale?

A

1) COPD causes chronic hypoxemia & acidosis
2) Pulmonary artery vasoconstriction
3) Increased pulmonary artery pressure
4) Irreversible until this point
5) Fibrosis & hypertrophy of smooth muscle layer of pulmonary arteries
6) Chronic pulmonary hypertension
7) Cor pulmonale
8) Right heart failure

69
Q

What is asthma?

A
  • Chronic inflammatory disorder of the airways
  • Characterised by reversible airflow obstruction causing cough, wheeze, chest tightness & SOB
  • Causes reversible bronchial hyper-responsiveness, constriction of the airways and variable airflow obstruction
70
Q

What are risk factors for asthma?

A
  • Cause of asthma not understood

- Genetic predisposition with environmental exposure to inhaled substances e.g. smoke, allergen, chemicals

71
Q

What is the pathophysiology of asthma?

A
  • Reversible airway obstruction
  • Dyspnea
  • Wheeze
  • Early response -bronchoconstriction
  • Last phase up to 6 hours later is inflammation and bronchoconstriction
  • IgE causes masts cells to degranulate, releasing inflammatory markers
72
Q

What is the pathophysiology of an exacerbation of asthma?

A

During exacerbation:

  • Bronchial hyperactivity
  • Smooth muscle cells in the bronchi constrict
  • Airways inflamed and swollen
  • Mucus plugs
73
Q

How to prevent asthma?

A
  • Reduce exposure to allergens
  • Lower air pollution
  • Smoking cessation
  • Immunisation
  • Lower occupational exposure
74
Q

What are pharmacotherapy management of asthma?

A
  • Mild - SABA inhalers
  • Persistent - anti-inflammatory medications & ICS
  • Not adequately controlled on ICS - Leukotriene antagonists
  • Severe - LABA
  • Oral NSAID
75
Q

What are non-pharmacological treatments of asthma?

A
  • Oxygen therapy
  • Monitoring of gas exchange & airway
    obstruction in response to therapy
  • Education
  • Skin Prick Testing for allergies

214.201 (17 decks)

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