Respiratory System (+pathophysiology) Flashcards

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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
Q

Function of surfactant?

A

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
Q

Lung compliance

A

Ability of kings to expand/ stretch (COMPLIANCE with its job of elasticity)

27
Q

Respiration equation

A

Glucose + 02 —> ATP, water, CO2

28
Q

Areas of the brain that control breathing

A

Medulla oblongata
Pons
(In brain stem)

29
Q

What causes respiratory conditions relating to chest wall

A

Trauma
Pneumothorax
Surgery

30
Q

What causes respiratory conditions relating to respiratory control centre

A

Raised ICP
Stroke
Opiates
Tumours
Head injury

31
Q

Causes of respiratory conditions relating to ventilation

A

Cystic fibrosis
Bronchitis
Asthma
Inhaled foreign body

32
Q

Causes of respiratory conditions relating to gas transfer

A

Oedema
Emphysema
Haemothorax
Lung cancer
Heart failure
Pulmonary thromboembolism
Sickle cell anaemia

33
Q

Potential causes of respiratory infections

A

Cilia (can’t move mucous)
Mucous overproduction
Loss of cough reflex
Pulmonary congestion/ oedema
Interference of white blood cells in alveolus

34
Q

Treatment for respiratory failure?

A

Oxygen supplement
Bronchodilators/corticosteroids for airway constriction
Diuretics for oedema/fluid build up
Mucolytics
Antibiotics for infection

35
Q

Respiratory failure?

A

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
Q

Type 1 respiratory failure?

A

Most common
Lungs unable to facilitate oxygen gas exchange (hypoxaemic)
Associated with acute lung diseases eg pneumonia/PE

37
Q

What is the value of Pa02 in an individual with type 1 respiratory failure?

A

<0.8 kPa
Normal- above 10.7 kPA

38
Q

Type 2 respiratory failure?

A

Failure of lungs to eliminate CO2, hypercapnic.
High PaCO2, low Pa02
Hypoxaemia common with this

39
Q

Causes of type 2 respiratory failure?

A

Emphysema
Asthma
Chronic bronchitis
Drug overdose (opiates)
Chest wall abnormalities
Neuromuscular disease

40
Q

Homeostasis (chemical) process for respiration

A

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
Q

Process that prevents over inflation of lungs (baroreceptors…)

A

Lungs inflate, baroreceptors in lung tissue detect pressure change (inflation)
Send sensory impulses to medulla
Impulses depress respiratory centre (prevents inflation, causes expiration)

42
Q

Peripheral chemoreceptors involved in detecting CO2/02/pH changes?

A

Aortic (vagus nerve) and carotid - send nerve impulses to brain via brainstem

43
Q

Respiratory centre?

A

Medulla

44
Q

Myasthenia gravis

A

Autoimmune disease (body attacks self)- destroys communication between nerves and muscles, lose voluntary control of muscles, no cure but there is treatment

45
Q

Ventilation vs perfusion

A

Ventilation- the volume of air moving in/out of mouth
Perfusion- volume of air in bloodstream/tissues (delivering oxygen)

46
Q

Pathologies that cause high V/Q ratio (high resp rate, low perfusion)

A

Heart failure

47
Q

Pathologies that cause a low V/P mismatch (less air moved in/out, low perfusion)

A

COPD

48
Q

Shunt in lungs + causes of this?

A

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
Q

Normal V/Q ratio?

A

0.8
Below= respiratory disorder that has caused a shunt?

50
Q

Cardiogenic Pulmonary oedema

A

-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
Q

Signs/ symptoms of pulmonary oedema

A

DIB
High resp rate
Coughing up pink frothy sputum
Cyanosis/hypoxia/pale skin
Fatigue/weakness
Oedema of ankles
Orthopnoea (breathless when lying down)

52
Q

Acute respiratory distress syndrome

A

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
Q

Causes of ARDS

A

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
Q

3 phases of ARDS

A

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
Q

Asthma

A

Chronic disorder, reaction to inhaled allergens/triggers:
Bronchospasm
Bronchoconstriction
Increased mucous secretion

56
Q

Pneumonia (+symptoms)

A

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