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Respiratory System (+pathophysiology) Flashcards

1
Q

COPD conditions

A

Emphysema, chronic bronchitis

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2
Q

Name of the enzyme that acts on the lungs

A

Protease

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3
Q

Protease action in lungs

A

Immune function- destroys pathogens
Lung disease- degradation of elastin in alveoli, causes COPD
Mucous secretion- goblet cells in airway
Inflammation in airways

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4
Q

Causes of emphysema/ chronic bronchitis

A

Inhaled irritants
Smoking
Pollution
Genetics
Age

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5
Q

Explain emphysema

A

Damage to alveoli, reducing surface area (elastin damaged= less elasticity/ lung compliance). Less oxygen is able to diffuse into the blood, air trapped in alveoli so less is exhaled.

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6
Q

Signs/symptoms of emphysema

A

Pink puffer (more effort in breathing)
Pursed lips (More effort in trying to remove C02)
SOB
Green/yellow sputum with cough
Tachycardia
Tachypnoea
Barrel chest
Accessory muscle use

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7
Q

Treatment for COPD

A

Oxygen supplement
Bronchodilators to manage airway constriction/ obstruction
Stop smoking
Mucolytics (break down excessive phlegm)

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8
Q

Why does smoking cause COPD ? (Effects of smoking on body)

A

Irritants in cigarettes stimulate protease activity in lungs (damage elasticity)
Smoke damages cilia in throat (unable to move mucous)
Inflammation/irritation of lungs stimulates goblet cells/ epithelial cells in airway to secrete mucous

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9
Q

Diagnosis of COPD

A

Spirometry
(Calculate FEV1/ FVC)
Below 0.70 = COPD

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10
Q

FEV1?

A

Forced expiratory volume in 1 second
(Maximum volume of air that can be forced out after a full breath in 1 second)

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11
Q

FVC?

A

Forced vital capacity
(Maximum volume of air that can be exhaled after taking a deep breath)

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12
Q

Chronic bronchitis?

A

Long term inflammation of the bronchi
Mucous secretion

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13
Q

Symptoms of chronic bronchitis

A

SOB, tachycardia, tachypnoea, blue bloater (cyanosis), pulmonary hypertension, chronic productive cough, accessory muscle use, low SATS

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14
Q

Tidal volume

A

Volume of air that moves in and out of the lungs during a single breath

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15
Q

Vital capacity

A

Maximum amount of air that can be expired after a deep breath in

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16
Q

Conducting zone

A

Mouth, nose, pharynx, larynx, trachea, bronchi, bronchioles
(Transport 02 to respiratory zone)

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17
Q

Respiratory zone

A

Where gas exchange occurs in the alveoli (02 into bloodstream, CO2 out)

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18
Q

Dead space

A

Air that isn’t used in gas exchange

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19
Q

Anatomical dead space

A

The volume of air in the conducting zone that is not used in gas exchange

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20
Q

Physiological dead space

A

Anatomical dead space + volume of air in the alveoli that is not used in gas exchange (alveolar dead space)

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21
Q

Value of alveolar dead space in a normal person vs unhealthy?

A

Normal- 0
Unhealthy- Alveolar dead space increases (greater than anatomical dead space)
Use physiological dead space clinically to indicate lung status

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22
Q

Inspiration action of body

A

External intercostal muscles contract, move rib cage outwards and upwards
Diaphragm muscle contracts and flattens
Volume increase, pressure decrease in thoracic cavity, air moves in

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23
Q

Expiration actions of body

A

Internal intercostal muscles contract, move rib cage downwards and inwards
Diaphragm relaxes to dome shape
Volume decreases, pressure increases
Air is forced out of the thoracic cavity

24
Q

Surfactant ?

A

Fluid that lines alveoli (contains lipids and proteins)

25
Function of surfactant?
Reduces surface tension in alveoli, prevents lungs from collapsing Defends against infection/ inflammation of lungs (proteins in fluid bind to bacteria/viruses and stimulate phagocytosis)
26
Lung compliance
Ability of kings to expand/ stretch (COMPLIANCE with its job of elasticity)
27
Respiration equation
Glucose + 02 —> ATP, water, CO2
28
Areas of the brain that control breathing
Medulla oblongata Pons (In brain stem)
29
What causes respiratory conditions relating to chest wall
Trauma Pneumothorax Surgery
30
What causes respiratory conditions relating to respiratory control centre
Raised ICP Stroke Opiates Tumours Head injury
31
Causes of respiratory conditions relating to ventilation
Cystic fibrosis Bronchitis Asthma Inhaled foreign body
32
Causes of respiratory conditions relating to gas transfer
Oedema Emphysema Haemothorax Lung cancer Heart failure Pulmonary thromboembolism Sickle cell anaemia
33
Potential causes of respiratory infections
Cilia (can’t move mucous) Mucous overproduction Loss of cough reflex Pulmonary congestion/ oedema Interference of white blood cells in alveolus
34
Treatment for respiratory failure?
Oxygen supplement Bronchodilators/corticosteroids for airway constriction Diuretics for oedema/fluid build up Mucolytics Antibiotics for infection
35
Respiratory failure?
Lungs are unable to remove carbon dioxide/exchange oxygen effectively due to dysfunction in respiratory system eg alveoli/ chest wall/ airways/ CNS/ pulmonary circulation
36
Type 1 respiratory failure?
Most common Lungs unable to facilitate oxygen gas exchange (hypoxaemic) Associated with acute lung diseases eg pneumonia/PE
37
What is the value of Pa02 in an individual with type 1 respiratory failure?
<0.8 kPa Normal- above 10.7 kPA
38
Type 2 respiratory failure?
Failure of lungs to eliminate CO2, hypercapnic. High PaCO2, low Pa02 Hypoxaemia common with this
39
Causes of type 2 respiratory failure?
Emphysema Asthma Chronic bronchitis Drug overdose (opiates) Chest wall abnormalities Neuromuscular disease
40
Homeostasis (chemical) process for respiration
High co2/acidic pH detected by chemoreceptors in medulla. Chemoreceptors send nerve impulses to respiratory centres in medulla. Chemoreceptors fire more frequently due to decreased pH, more nerve impulses to respiratory centres, respiratory muscles activated more frequently to contract (ventilation) C02 released Body stimulated to increase respiratory rate
41
Process that prevents over inflation of lungs (baroreceptors…)
Lungs inflate, baroreceptors in lung tissue detect pressure change (inflation) Send sensory impulses to medulla Impulses depress respiratory centre (prevents inflation, causes expiration)
42
Peripheral chemoreceptors involved in detecting CO2/02/pH changes?
Aortic (vagus nerve) and carotid - send nerve impulses to brain via brainstem
43
Respiratory centre?
Medulla
44
Myasthenia gravis
Autoimmune disease (body attacks self)- destroys communication between nerves and muscles, lose voluntary control of muscles, no cure but there is treatment
45
Ventilation vs perfusion
Ventilation- the volume of air moving in/out of mouth Perfusion- volume of air in bloodstream/tissues (delivering oxygen)
46
Pathologies that cause high V/Q ratio (high resp rate, low perfusion)
Heart failure
47
Pathologies that cause a low V/P mismatch (less air moved in/out, low perfusion)
COPD
48
Shunt in lungs + causes of this?
Under ventilated areas of the lungs, causes low oxygen levels in venous blood returning to the heart Causes: pneumonia, atelectasis (collapsed alveoli), pulmonary oedema
49
Normal V/Q ratio?
0.8 Below= respiratory disorder that has caused a shunt?
50
Cardiogenic Pulmonary oedema
-Heart pumps blood inefficiently due to left sided heart failure- weakened ventricle muscles), causes a backlog of fluid/blood to build up in pulmonary veins Rise in hydrostatic pressure causes pulmonary oedema (fluid leaks into lungs) -can also be caused by disease of heart valves
51
Signs/ symptoms of pulmonary oedema
DIB High resp rate Coughing up pink frothy sputum Cyanosis/hypoxia/pale skin Fatigue/weakness Oedema of ankles Orthopnoea (breathless when lying down)
52
Acute respiratory distress syndrome
Form of non cardiogenic pulmonary oedema (not caused by heart failure) Can lead to acute respiratory failure as fluid builds up in lungs/alveoli, stiffens lungs More pro inflammatory mediators than anti inflammatory, causes inflammation
53
Causes of ARDS
Infection eg pneumonia, sepsis Acute lung injury (triggers immune response, inflammation, neutrophils, increased vascular permeability causing pulmonary oedema) PE Drowning, trauma (chest injury) Severe burns
54
3 phases of ARDS
1) Exudative phase (first 24 hours, hypoxaemic, fluid leakage into alveoli, neutrophils respond) 2) Proliferative phase (2 weeks after, reduced lung compliance/surfactant), thrombi form in lungs 3) Fibrotic phase (3 weeks, widespread pulmonary fibrosis, loss of lung compliance/elasticity, loss of lung structure
55
Asthma
Chronic disorder, reaction to inhaled allergens/triggers: Bronchospasm Bronchoconstriction Increased mucous secretion
56
Pneumonia (+symptoms)
Infection via bacteria/virus Inflammation of lung (action of white blood cells in alveoli, pus formation- dead cells) Symptoms: -SOB -coughing green/yellow phlegm -chest pain that worsens with breathing -fever/chills

Paramedic Science (9 decks)

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