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RS Flashcards

0
Q

What is vital capacity?

A

The greatest volume of air that can be exhaled from the lungs after taking the deepest possible breath

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1
Q

What is the vital capacity used to measure?

A

Lung volume

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2
Q

What is the parasympathetic neurotransmitter in the lung?

A

Acetylcholine

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3
Q

What is the sympathetic neurotransmitter in the lung?

A

Noradrenaline

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4
Q

Where are the frontal sinuses?

A

Within the frontal bone, in the midline septum, but this may not be in the midline. Over the orbit and across the superciliary arch.

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5
Q

What is the nerve supply of the frontal sinuses?

A

The ophthalmic branch of the trigeminal nerve

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6
Q

Where are the paranasal sinuses?

A

Pneumatised areas of the frontal, maxillary, ethmoid and sphenoid bones. They are arranged in pairs.

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7
Q

What are the paranasal sinuses?

A

The are envaginations of the mucous membrane from the nasal cavity. They are lined with cilia

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8
Q

What are the functions of the nose?

A

It regulates temperature and humidity of inspired air; it has a filter function (mammals are obligate nasal breathers); it has a defence function ( lined with cilia)

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9
Q

Where does the anterior nares lead to?

A

The anterior nares (nostrils) open into the enlarged vestibule (skin-lined and has stiff hairs).

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10
Q

What do the turbinates do?

A

They double the surface area of the nose. They create the superior, middle and inferior meatus’

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11
Q

Where are the maxillary sinuses?

A

They are located within the body of the maxilla. They are a pyramidal shape.

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12
Q

What is the base of the maxillary sinuses?

A

The lateral wall of the nose

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13
Q

What is the apex of the maxillary sinuses?

A

The zygomatic process of the maxilla

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14
Q

What is the roof of the maxillary sinuses?

A

The floor of the orbit

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15
Q

What is the floor of the maxillary sinuses?

A

The alveolar process

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16
Q

Where do the maxillary sinuses open into?

A

The Middle meatus via the hiatus semilunaris. They train all the liquid into the middle meatus

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17
Q

Where are the ethmoid sinuses?

A

They are between the yes. They are a labyrinth of air cells

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18
Q

What is the nerve supply of the ethmoid sinuses?

A

The ophthalmic and maxillary branches of the trigeminal nerve

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19
Q

Where are the sphenoid sinuses?

A

Medial to the cavernous sinus and inferior to the optic canal, dura and pituitary gland

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20
Q

Where do the sphenoid sinuses empty into?

A

The sphenoethmoidal recess, lateral to the attachment of the nasal septum

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21
Q

What is the nerve supply of the sphenoid sinuses?

A

The opthalmic branch of the trigeminal nerve

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22
Q

What is the pharynx?

A

It is a fibromuscular tube that goes from the skull base to the oesophagus. It consists of the nasopharynx, oropharynx and laryngopharynx

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23
Q

What is the epithelium of the pharynx?

A

It is lined with squamous and ciliated epithelium with interspersed mucous glands

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24
Q

Where is the nasopharynx?

A

It is bound by the base of the skull, the sphenoid rostrum, C spine, posterior nose and opens into the oropharynx.

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25
Q

Where are the pharyngeal tonsils?

A

They are located on the posterior wall of the nasopharynx

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26
Q

Where do the eustacian tube orifices open into?

A

The lateral wall of the nasopharynx to supply air to the middle ear

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27
Q

What is the oropharynx?

A

It is a tube to take air from the aural cavity into the lung

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28
Q

What is the oropharynx bound by?

A

The soft palate anteriorly. The hyoid bone superiorly. It goes from the nasopharynx to the laryngopharynx

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29
Q

Where are the palatine tonsils?

A

The palatine tonsils are on the lateral walls of the oropharynx. The palatoglossal folds are the anterior arches and the palatopharyngeal folds are the posterior arches

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30
Q

What are the types of laryngeal cartilages?

A

Single and double. There are 9 in total.

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31
Q

What are the single laryngeal cartilages?

A

The epiglottis, the thyroid cartilage and the cricoid cartilage

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32
Q

What are the double laryngeal cartilages?

A

The cuneiform cartilages, the corniculate cartilages and the arytenoid cartilages

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33
Q

What is the function of the larynx?

A

It has a valvular function so prevents liquids and food entering the lungs.

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34
Q

What is the structure of the larynx?

A

It has a rigid structure made of multiple muscles and 9 cartilages.

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35
Q

What nerves is the larynx innervated by?

A

It is supplied by vagus branches: the superior and recurrent laryngeal nerves.

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36
Q

What is the path of the superior laryngeal nerve?

A

It comes from the inferior ganglion down the lateral pharyngeal wall and divides into the internal (sensation) and external (cricothyroid muscle) superior laryngeal nerves.

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37
Q

What does the recurrent laryngeal nerve supply?

A

It supplies all muscle but the cricothyroid. It ascends between the trachea and oesophagus

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38
Q

What are the components of the lower respiratory tract?

A

It is below the stern all angle. It consists of the pleura and the main airways: the trachea, the main bronchi, the lobar bronchi, the segmental bronchi, the terminal bronchioles, the respiratory bronchioles, the alveolar ducts and the alveoli

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39
Q

What is the function of the lower respiratory tract?

A

It’s main function is gas exchange. It has 20m2 gas exchange area per lung. The minute ventilation and cardiac output are approx. 5L/min. There are regional differences in ventilation and perfusion

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40
Q

Where is the trachea?

A

It is from the larynx to the carina, which is at T5 level.

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41
Q

What shape is the trachea?

A

It is oval-shaped with semi circular cartilages

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42
Q

What is the lining of the trachea?

A

Pseudo-stratified, ciliated columnar epithelium with interspersed goblet cells

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43
Q

What are the two main bronchi?

A

The trachea splits into the right main bronchi and the left main bronchi at the carina.

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44
Q

What is the difference between the left main bronchus and the right main bronchus?

A

The left main bronchus is a lot less verticle and is longer. It is 5cm long and it related to the aortic arch. The right main bronchus is 1-2.5cm long and is related to the right pulmonary artery

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45
Q

What is antibody opsonisation?

A

It is the process by which a pathogen is marked for ingestion and eliminated by a phagocyte

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46
Q

What is a cough?

A

A cough is an explosive expiration that provides a normal protective mechanism for clearing the tracheobronchial tree of secretions and foreign material

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47
Q

How main lobar bronchi are there?

A

3 on the right (upper, middle and lower) and 2 on the left (upper and lower).

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48
Q

What is the acinus?

A

It is the area distal to the terminal bronchiole. The short tube ducts with multiple alveoli

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49
Q

What are the pores of Kohn?

A

The interconnections between the alveoli

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50
Q

What are the components of alveoli?

A

There is a basement membrane, interstitial tissue and capillary endothelial cells. There are also alveolar macrophages

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51
Q

What are the two types of alveoli?

A

Type 1 pneumocytes, which cover 90-95% of the surface and aid gas exchange. Type 2 pneumocytes, which cover 5-10% of the surface and decrease surface tension and secrete surfactant

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52
Q

What does lung innervation control?

A

Many aspects of function; smooth muscle tone, mucous gland secretion, blood flow and vascular permeability

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53
Q

What does sympathetic innervation of the lung cause?

A

Bronchodilation

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54
Q

What does parasympathetic innervation of the lung cause?

A

Bronchoconstriction

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55
Q

What are the two circulation systems in the lung?

A

There are bronchial and pulmonary circulation systems

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56
Q

What are the muscles of inspiration?

A

Largely due to the diaphragm (C3,4,5) and external intercostals (nerve roots at each level)

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57
Q

What are the muscles of expiration?

A

It is passive during quiet breathing

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58
Q

What is the motor innervation of respiration?

A

The diaphragm is innervated by C3,4,5 and the internal intercostals are innervated by thoracolumbar nerve roots at each level

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59
Q

What is the sensory innervation of respiration?

A

There are afferents via the vagus nerve. There are sensory receptors. There are C fibres (small nerve fibres)

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60
Q

Where is resistance highest in the respiratory airways?

A

In the main airways, terminal bronchi

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61
Q

What is dead space?

A

Areas of the lung where air is supplied but no gas exchange takes place

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62
Q

What are the two layers of lung pleura?

A

Visceral (applied to the lung surface) and parietal (applied to the internal chest)

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63
Q

What is the visceral pleura innervated by?

A

It is only innervated by autonomic innervation

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64
Q

What sensation does the parietal pleura have?

A

It only senses pain

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65
Q

How thick are the lung pleura?

A

They are only a single cell later but they are continuous with each other at the lung root. There is a small amount of fluid between the layers

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66
Q

What properties of the lug allow expiration?

A

Both the chest wall and the lungs have elastic properties and a resting volume. Changing this volume requires force. Release of this force leads to a return to the resting volume

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67
Q

When are capillaries perfused with blood?

A

They are the most dependant parts of the lung and are preferentially perfused with blood at rest

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68
Q

What affects the perfusion of capillaries?

A

It depends on pulmonary artery and venous pressure. Certain pulmonary arteries have smooth muscle within their walls which create resistance

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69
Q

What is the PaCO2?

A

The arterial CO2

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70
Q

What is the PACO2?

A

The alveolar CO2

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71
Q

What is the PaO2?

A

The arterial O2

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72
Q

What is the PAO2?

A

The alveolar O2

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73
Q

What is the PIO2?

A

The pressure of inspired oxygen

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74
Q

What is the V’A?

A

The alveolar ventilation

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75
Q

What is the V’CO2?

A

The CO2 production

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76
Q

What are the oxygenation sites in the lung?

A

The alveolar epithelium, the tissue interstitium, the capillary endothelium, the plasma layer, the red cell membrane, the red cell cytoplasm and the Hb binding forces

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77
Q

What are the causes of hypoxaemia?

A

Alveolar hypoventilation, reduced PIO2, diffusion abnormality, ventilation/perfusion mismatch

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78
Q

How is CO2 transported?

A

It binds to Hb, or it is dissolved in the plasma or it reacts with H2O to form HCO3-

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79
Q

How is PaCO2 calculated?

A

kV’CO2/V’A = PaCO2

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80
Q

What is the Henderson-Hasselbach equation?

A

pH = 6.1* + log10([HCO3-][0.03*PCO2])

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81
Q

What is * in the Henderson-Hasselbach equation?

A

A dissociation constant

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82
Q

What is 0.03*PCO2 in the Henderson-Hasselbach equation?

A

The estimate of H2CO3

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83
Q

How is change in pressure worked out?

A

Flow x resistance

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84
Q

What is laminar flow?

A

It is low velocity / density. The change is pressure is proportional to the flow

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85
Q

What are the lung defence mechanisms?

A

There are innate immune mechanisms; non-immune mechanisms; adaptive mechanisms

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86
Q

What are epithelial chemical barriers?

A

Antiproteinases; anti-fungal peptides (alpha defensins); anti-microbial peptides (beta defensins); surfactant -A and -D proteins opsonise pathogens

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87
Q

How does turbulent flow affect pressure?

A

The change in pressure is proportional to the flow squared

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88
Q

What is poiseuilles law?

A

Airways resistance is proportional to the fourth power of the radius

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89
Q

What are some acid-base disorders?

A

Respiratory acidosis; respiratory alkalosis; metabolic acidosis; metabolic alkalosis

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90
Q

What is respiratory acidosis?

A

Increased PaCO2, decreased pH, mild increase HCO3- (barely breathing)

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91
Q

What is respiratory alkalosis?

A

Decreased PaCO2, increased pH, mild decrease HCO3- (heavy breathing)

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92
Q

What is metabolic acidosis?

A

Reduced HCO3-, decreased pH

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93
Q

What is metabolic alkalosis?

A

Increased HCO3-, increased pH

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94
Q

What is FEV1?

A

Forced expiratory volume in one second

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95
Q

What is FVC?

A

Forced vital capacity

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96
Q

What is PEF?

A

Peak expiratory flow

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97
Q

What is boyles law?

A

At a constant temperature for a fixed mass, the absolute pressure and the volume of a gas are inversely proportional

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98
Q

What is the peak expiratory flow?

A

It is a single measure of the volume expired in the first 0.1 second of forced expiration in L/min

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99
Q

What are the bad things about the peak expiratory flow?

A

It is less reproducible than FEV1. It is very effort dependant.

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100
Q

What is gas dilation?

A

It is a measurement of all air in the lungs that communicates with the airways. It doesn’t measure air in non-communicating bullae.

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101
Q

How does gas dilation work?

A

It uses open-circuit nitrogen washout. Give the patient a known concentration of gas, take gas from them and measure the difference. The patient breathes 100% oxygen and all the nitrogen in the lung is washed out

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102
Q

What is FEF25?

A

The flow at the point when 25% of the total volume to be exhaled has been exhaled

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103
Q

How is forced expiration measured?

A

Breathe into total lung capacity, exhale as fast as possible to residual volume, the volume produced is the vital capacity.

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104
Q

How does expiration vary during forced expiration?

A

There is rapid exhalation in the first second, it takes 4 seconds to empty your lungs because of the elastic recoil

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105
Q

How does FEV change with age

A

It takes longer as your get older

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106
Q

How does flow differ with volume?

A

The flow is greatest at the start of exhalation. The volume declines linearly with flow, as the volume decreases, the flow does

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107
Q

What does exhaled nitric oxide measure?

A

An indirect reflection of airways inflammation. Exhaling from total lung capacity into gas analyser under positive expiratory pressure. 5-20ppb is normal. There are nasal NO issues

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108
Q

How does airways resistance vary?

A

An increase in turbulence increases resistance. At total lung capacity, resistance is low. During expiration airway diameter decreases and resistance increases.

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109
Q

What is conductance?

A

It is the opposite of resistance

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110
Q

What is lung compliance?

A

It is the change in volume per unit change in pressure gradient between the pleura and alveoli (transpulmonary pressure) it can be static or dynamic

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111
Q

What is static compliance?

A

It is a measure of distensibility. A lung of high compliance expands more at a constant transpulmonary pressure.

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112
Q

What is dynamic compliance?

A

It is measured during tidal breathing after inspiration and expiration when lungs are stationary. It is only less than static compliance when there is respiratory obstruction

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113
Q

What is DLco?

A

It measures the interaction of: alveolar SA, alveolar capillary perfusion, alveolar capillary interface, capillary volume, Hb concentration and the CO and Hb reaction rate. It is the rate of uptake of CO/pressure of CO

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114
Q

How is the DLco measured?

A

It is a single 10 second breath-holding technique. The alveolar sample is obtained & DLco is calculated from the total volume of the lung, breath-hold time and initial and final [CO]

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115
Q

How is flow measured?

A

Anemometer; hot wire detector; baffle; pneumotachograph

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116
Q

What does an anemometer do?

A

It counts vane rotation

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117
Q

What does a hot wire detector do?

A

It measures cooling, which is proportional to flow

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118
Q

How does a baffle work?

A

The distance the baffle moves is proportional to flow

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119
Q

How does a pneumotachograph work?

A

Air flows through lots of thin tubes, the pressure is measured in two places. The drop in pressure is proportional to flow

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120
Q

Why should you measure lung function?

A

To make a diagnosis; to monitor a known disease (progress of the disease, effect of treatment, effect of exposures); disability evaluation

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121
Q

What are the good points about FEV1?

A

It is highly reproducible, it is a good overall assessment of lung health, it is a good overall assessment of mortality risk. Over 80% is normal

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122
Q

What does FVC indicate?

A

A value of under 80% indicates airway restriction. But it is less reproducible than FEV1

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123
Q

What is the FEV1/FVC ratio?

A

It measures the percentage of total lung volume exhaled in the first second. Less than 70% is abnormal.

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124
Q

What does FEV1/FVC indicate?

A

A low FEV1/FVC (less than 70%) shows airway obstruction. A normal ratio and low FVC shows airway restriction

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125
Q

What are the different types of cholinergic receptors?

A

Nicotinic (ganglia, neuromuscular junctions) and muscarinic (parasympathetic, M1,2,3,4,5)

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126
Q

What are the types of adrenergic receptors?

A

Alpha and beta(1,2,3)

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127
Q

Where are beta-1-adrenergic receptors?

A

In the heart

128
Q

Where are beta-2-adrenergic receptors?

A

In the lung

129
Q

Where are the beta-3-adrenergic receptors?

A

In adipose tissue

130
Q

What are the types of receptor communication?

A

Neurotransmitter (ACh, NAd) Hormones (testosterone) Autacoids (histamine)

131
Q

What are autacoids?

A

In between hormones and neurotransmitters. Messengers that aren’t found in nerves.

132
Q

What are the types of receptor?

A

G-protein coupled receptors (muscarinic, adrenergic); receptors linked to ion channels (nicotonic); nuclear receptors (steroid)

133
Q

What is the parasympathetic neurotransmitter of the lung?

A

Acetylcholine

134
Q

What is the sympathetic neurotransmitter of the lung?

A

Noradrenaline

135
Q

What parts of the lung are innervated?

A

The vasculature and glands are both sympathetic and parasympathetically innervated. Whereas the airways are only parasympathetically innervated

136
Q

How is intrinsic tone of the lung innervated?

A

Intrinsic tone is due to parasympathetic ACh reacting with cholinergic receptors on the smooth muscle in the airways, causing bronchoconstriction

137
Q

How is extrinsic tone innervated in the lungs?

A

It is indirectly influenced by the hypothalamus to the adrenal gland, which secretes adrenaline following sympathetic activation, causing bronchodilation

138
Q

What are the types of ligand receptors?

A

Agonist and antagonist

139
Q

What is an agonist?

A

A compound that binds to a receptor and activates it, affinity and efficacy are both shown. Examples include: muscarine mAChR and nicotine nAChR

140
Q

What is an antagonist?

A

A compound that blocks the effect of an agonisist. Affinity is shown but it has no efficacy. Examples include atropine mAChR

141
Q

What does affinity mean?

A

How well the ligand binds to the receptor

142
Q

What does efficacy mean ?

A

How well it activates the receptor

143
Q

How does an agonist activate a G protein coupling receptors?

A

An agonist binds to and causes a shape change of the receptor so it is activated. The receptor then couples with a G protein, which leads to enzyme activation.

144
Q

What type of receptors des ACh activate?

A

Muscarinic receptors

145
Q

What type of receptor does noradrenaline activate ?

A

Beta-2-adrenoreceptors

146
Q

How does the muscarinic receptor affect the lungs?

A

The muscarinic 3 receptor is activated by ACh, this creates IP3 & DAG, which activates PKC and increases Ca2+, which causes bronchoconstriction

147
Q

How does noradrenaline affect the lung?

A

It activates beta-2-adrenoreceptors, which creates cyclic AMP, which activates PKA and causes bronchodilation

148
Q

Where does the pulmonary circulation come from?

A

It is 100% of the blood flow from the right ventricle

149
Q

Where is the bronchial circulation come from?

A

It is 2% of the left ventricular output

150
Q

What is Pouiseuille’s law?

A

(8L x viscosity) / Pi(r4)

151
Q

What is Ohm’s law?

A

V = I x R Cardiac output = (mPAP - LAP) / PVR mPAP (mean pulmonary artery pressure) LAP (left arterial pressure) PVR (pulmonary vascular resistance)

152
Q

What is type 1 pulmonary failure?

A

Low pO2 Low pCO2

153
Q

What is type 2 respiratory failure?

A

Low pO2 High pCO2

154
Q

What are the causes of hypoxaemia?

A

Hypoventilation (failure to ventilate), diffusion impairment, shunting (blood bypasses the lungs), V/Q mismatch (parts of the lung with the most blood ventilate the least)

155
Q

What causes diffusion impairment?

A

It can be gaseous (pulmonary oedema); blood (anaemia); membrane (interstitial fibrosis)

156
Q

What are some pulmonary circulation problems?

A

V/Q mismatch (pulmonary oedema); increased pulmonary vascular resistance (pulmonary arterial hypertension); shunting (pulmonary arteriovenous malformation)

157
Q

What are the world bank regions?

A

The world bank divides countries into 4 income grouped based on GNP per person: low; lower middle; higher middle and high

158
Q

What is public health?

A

Data and evidence to support action, it focuses on populations, social justice and equity. The emphasis is on prevention rather than cure

159
Q

What is international health?

A

The diseases and conditions of middle and low income countries

160
Q

What is global health?

A

It transcends national boundaries, requiring greater interdisciplinary approach

161
Q

What are the components of the breathing system?

A

Sensors -> central controllers -> effectors (muscles)

162
Q

Name 5 of the millennium development goals?

A
  1. Reduce child mortality 2. Improve maternal health 3. Ensure environmental sustainability 4. Combat HIV/AIDS, malaria and other diseases 5. Achieve universal primary education
163
Q

Where are the brain stem respiratory centres?

A

The medulla and the pons

164
Q

What does the medulla respiratory centre control?

A

It controls normal breathing. It is affected by the cortex, emotions from the limbic system, chemoreceptors, stretch receptors and proprioreceptors

165
Q

Where is the pneumotaxic area?

A

It is in the upper pons. It causes quick, shallow breathing by switching off inspiration neurones to prevent hyperinflation, allowing lots of expiration

166
Q

Where is the apneustic area?

A

It is in the lower pons. It sends messages to the inspiration neurones activating them to inhibit expiration and cause fewer, deeper breaths. It is overridden by the pneumotaxic area

167
Q

What are C fibres J receptors?

A

Thy are sensory nerve endings located within the alveolar walls. They are activate by an increase in interstitial fluid.

168
Q

What do C fibres J receptors do?

A

Activity causes rapid, shallow breathing, bronchoconstriction and cardiovascular depression

169
Q

What is respiratory epithelium?

A

It is pseudostratified, ciliated epithelial cells interspersed with goblet cells. It lines the tubular portion of the respiratory system

170
Q

What receptors are is the nose, nasopharynx and larynx?

A

Chemo and mechano receptors. Some appear to sense and monitor flow, stimulation of these receptors appears to inhibit the central controller

171
Q

What receptors are in the pharynx?

A

There are receptors that appear to be activated by swallowing, respiratory activity stops during swallowing to protect against the risk of food or liquid entering the lung

172
Q

What are the different types of pulmonary receptors?

A

C fibres J receptors, slowly adapting stretch receptors and rapidly adapting receptors

173
Q

Where are slowly adapting stretch receptors found?

A

In airway smooth muscle. They are activated by lung distension, high activity inhibits further inspiration, beginning expiration.

174
Q

Where are rapidly adapting stretch receptors?

A

They are found between airway epithelial cells, activated by lung distension and irritants. They produce a brief burst of activity, high activity causes bronchoconstriction

175
Q

What is the function of the nasopharynx?

A

It transports gas from the nose into the larger airways. It performs humidification, warming and olfaction. It is lined with respiratory epithelium

176
Q

What are the functions of the nasal sinuses?

A

They lower the weight of the skull, they add resonance to the voice, they humidify and warm inspired air, they are lined by respiratory epithelium

177
Q

What is the larynx?

A

It is a cartilaginous box that aids voice production

178
Q

What is the larynx made of?

A

Loose fibrocollagenous stroma with seromucous glands. Lymphatics and blood vessels are common. It is lined by respiratory epithelium

179
Q

What is the epithelium of the vocal cords?

A

It is stratified squamous epithelium overlying loose irregular fibrous tissue (Reinke’s space). There is almost no lymphatics

180
Q

What is the function of the trachea?

A

It conducts air to and from the lungs.

181
Q

What is the trachea made of?

A

It has C-shaped cartilagenous rings. It is lined with respiratory epithelium. It has seromucinous glands in the submucosa.

182
Q

What is the bronchi made of?

A

It has smooth muscle. It is lined by respiratory epithelium. It has some basal neuroendocrine cells. It has seromucous glands and goblet cells

183
Q

What are the bronchioles made of?

A

It has smooth muscle, it is lined by ciliated columnar epithelium. It has some basal neuroendocrine cells but few goblet cells. It also has Clara cells

184
Q

What are Clara cells?

A

They contain mitochondria, smooth ER, secretory granules and vesicular cytoplasm. They aren’t ciliated

185
Q

What is the function of the respiratory bronchioles?

A

It performs gas exchange as well as transport. It links terminal bronchioles and alveolar ducts. They are first part of the distal respiratory tract.

186
Q

What are the respiratory bronchioles made of?

A

Spirally arranged smooth muscle with no cartilage. They are lined by ciliated cuboidal epithelium

187
Q

What is the interstitium?

A

It is the cells between the alveoli, where endothelial cells are not in direct contact with pneumocytes. It contains collagen and elastin fibres, fibroblasts and macrophages

188
Q

What is the afferent innervation that causes coughing?

A

It includes receptors within the sensory distribution of CN V, IX, X

189
Q

What is the efferent innervation of coughing?

A

It is the recurrent laryngeal nerve and the spinal nerves

190
Q

How does coughing happen?

A

The epiglottis and vocal cords shut sharply to trap air in the lungs. The internal intercostal and diaphragm muscles contract so pressure increases. The epiglottis and vocal cords open and the pressure difference forces air out

191
Q

What function does epithelia have in lung defence?

A

Provide a physical and chemical barrier to prevent infection. Exhibits a remarkable ability to repair. The aberrant repair and reorganisation underpins many lung diseases

192
Q

What happens during necrosis?

A

The cell is swollen, the organelles are damaged and the chromatin is altered. The cell is lysed, the organelles are destroyed and the contents are released. There is inflammation.

193
Q

What happens during apoptosis?

A

The cell is shrunken, the organelles are undamaged and the chromatin is marginated. The apoptic bodies formed with the organelles in tact, the chromatin is fragmented and the contents retained. There is no inflammation

194
Q

What are the functions of neutrophils?

A

The receptor detects the pathogen. There is activation (signal transduction pathways). Marination is due to selectin. Adhesion is due to integrity. Chemotaxis, phagocytosis and bacterial killing (lysosomes and ROS)

195
Q

What is the function of alveolar macrophages?

A

They function as the resident phagocyte; the coordinate the inflammatory response and clearance of apoptic cells

196
Q

What are the differences between macrophages and myocytes?

A

Macrophages generate more ATP and have a lower susceptibility to apoptosis than monocytes

197
Q

How are macrophages formed?

A

The arise from monocytes, which come from bone marrow precursors. When the monocyte moves to the lung and alveoli it matures.

198
Q

What are the types of pattern recognition receptors (PRRs)?

A

Endocytotic and signalling receptors

199
Q

What are endocytotic receptors?

A

They promote phagocytosis without an intracellular signal. The examples are: mannose receptors; glucan receptors; scavenger receptors

200
Q

What are the types of signalling receptors?

A

NODs and Toll-like receptors (TLRs)

201
Q

What are NOD receptors?

A

They are cytoplasmic proteins that recognise inflammatory and apoptic receptors

202
Q

What are TLRs?

A

They recognise conserved molecular patterns in pathogens

203
Q

What are type 1 pneumocytes?

A

They are 40% of the cell population and 90% of the SA because it is squamous with not much cytoplasm. They are flattened cells with flattened nuclei and few organelles

204
Q

What are type 2 pneumocytes?

A

They are 60% of the cell population and 5-10% of the SA. They are rounded cells with a round nucleus, lots of organelles. They produce surfactant.

205
Q

What are alveolar macrophages?

A

They are luminal cells also present in the interstitium. They phagocytose particulates and enter lymphatics or leave via muscociliary escalator

206
Q

What epithelium does the nose have?

A

It has keratinising and non-keratinising squamous epithelium and respiratory epithelium.

207
Q

Where does olfaction take place?

A

In the roof of the nasal cavity, extending down the septum and lateral wall. It has pseudostratified columnar epithelium of olfactory receptor cells with supporting sustentacular and basal cells, along with serous glands of bowmans

208
Q

What is the pseudoglandular phase?

A

It is 5-17th week in the embryo. Major structural lung units are formed through angiogenesis

209
Q

What is the canalicular phase?

A

It is 16-25 weeks in the embryo. It is vascularisation of the lungs. Respiratory bronchioles and alveolar ducts are formed, creating the terminal sacs

210
Q

When does alveolarisation take place?

A

Between the 24th week in the embryo and birth alveolar cells (type 1 and 2) are formed. The alveoli are simple with thick interstitium. From birth to 3-5yrs old there is thinning of alveolar membrane and interstitium and the complexity of alveoli increases

211
Q

How does oxygen affect the diameter of vessels?

A

It is a vasoconstrictor of systemic vessels but a vasodilator of pulmonary vessels

212
Q

What is immunosenecesnce?

A

The decline in innate immune response and the adaptive immune response with age

213
Q

What is dyspnoea?

A

It is the sense of awareness of increases respiratory effort

214
Q

What is orthopnoea?

A

Breathlessness on lying down

215
Q

What is tachypnoea?

A

Increased respiratory rate

216
Q

What is bradypnoea?

A

Reduced respiratory rate

217
Q

What is hyperventilation?

A

Inappropriate heavy breathing

218
Q

What is paroxysmal nocturnal dyspnoea?

A

Episodes of shortness of breath

219
Q

What is extrinsic allergic alveolitis?

A

Inflammation of the alveoli caused to hypersensitivity of inhaled dusts. It is a type 3 reaction

220
Q

How do you work out PAO2?

A

PAO2 = PiO2 - PaCO2/R**

221
Q

How do you work out PaO2?

A

PaO2 = PAO2 - (A-aDO2) ( the difference between the alveoli and arterial pressure)

222
Q

What is barotrauma?

A

Injury resulting from volume changes to enclosed has spaces within or adjacent to the body. During descent it is in the ear, teeth and sinuses. During ascent it is in the lungs. It is affected by boyles law

223
Q

What is Henry’s law?

A

The amount of a gas dissolved in a liquid at a given temperature is directly proportional to the partial pressure of the gas over the liquid. It affects DCI (decompression illness)

224
Q

What is Dalton’s law?

A

The total pressure exerted by a mixture of gases is equal to the sum of the pressures that would be exerted by each of the gases if it was alone and occupied the total volume. It affects O2 toxicity and N2 narcosis

225
Q

What is heterozygote advantage?

A

When being a carrier of one disease gives added immunity to another disease (sickle cell anaemia and malaria)

226
Q

What is airways mucus made of?

A

It as a viscoelastic gel containing water, carbohydrates, proteins and lipids.

227
Q

Where is mucus made?

A

It is the secretory product of the mucous cells (goblet cells and submucosal glands)

228
Q

What is the function of mucus in the lungs?

A

It protects the epithelium from foreign material and fluid loss.

229
Q

How is mucus transported?

A

It is transported to the pharynx by airflow and the mucociliary clearance

230
Q

What are the two layers of mucus?

A

It consists of a superficial mucous later and a surfactant fluid layer, which bathes the epithelia.

231
Q

What affects the mucus layer?

A

The depth and composition depends on secretion, discharge and active ion transport across the epithelium

232
Q

What are the functions of the adaptive immune response?

A

It recognises specific non-self antigens. It generates responses tailored to eliminate specific pathogens. It develops immunological memory, at both individual and evolutionary levels. It allows a rapid response in the future

233
Q

What is a TCR?

A

It is the T cell receptor. It is made in the thymus.

234
Q

What are gamma delta T cells?

A

They have invariant TCRs that can act as PPRs. They are found at mucosal surfaces and recognise foreign cells.

235
Q

How do T cells get activated?

A

They circulate til they bind with an APC B cell. They are activated and differentiate into types of T cells

236
Q

What are the types of T cells?

A

T helper cells (CD4); Cytotoxic T cells (CD8); T memory cells (CD4); regulatory T cells (CD4/25); natural killer T cells (CD1d).

237
Q

What are the types of T helper cells?

A

T helper 1 cells function in bacterial infection; T helper 2 cells function in parasites or no infection; T helper 3 cells are regulatory cells.

238
Q

What are the 5 types of antibodies produced by B cells?

A

IgA, IgD, IgE, IgG, IgM. Each antibody recognises a specific epitope.

239
Q

What is an epitope?

A

Part of the protein that the antibody recognises

240
Q

What activates a B cell?

A

The unique B cell receptor is an immobilised antibody. When it is activated by a specific antigen & a T helper cell it becomes a plasma cell, secretes antibodies and triggers complement activation.

241
Q

What happens during chronic inflammation?

A

It replaces functional tissue with collagen. This knowledge helps with diagnosis and treatment.

242
Q

What causes chronic inflammation to be chronic?

A

(1) The initiating cause (mycobacteria) persists. (2) The cellular response is inappropriate. (3) there are structural abnormalities (diverticular disease)

243
Q

What are the three types of chronic inflammation?

A

Suppurative (puss forming); granulomatous (granula forming); autoimmune

244
Q

What does chronic inflammation cause?

A

Excessive fibrosis (strictures, adhesions) and growth disorders (metaplasia)

245
Q

What makes up the immune system?

A

Cells (phagocytic neutrophils and macrophages; antibody producing lymphocytes) and humoral (immunoglobulins; surfactant proteins; complement (formation of the membrane attack complex)

246
Q

What are cytokines?

A

Cytokines are proteins that allow tissue cells and leukocytes to talk to one another.

247
Q

What is adaptive immunity?

A

The formation of immunological memory. An example of vaccination: the APCs show antigens to lymphocytes. They support production of antibodies and also look for these molecules on tissue cells

248
Q

What is innate immunity?

A

It does not require prior exposure to recognise something’s gone wrong. It is mainly about eating bacteria and rapid responses to viruses.

249
Q

What is a type 1 immune reaction?

A

It involves IgE. It is immunological memory to something causing an allergic reaction.

250
Q

How quick are type 1 reactions?

A

They typically happen very fast, normally less than half an hour

251
Q

What is atopy?

A

It is the inherited tendency to exaggerated IgE response to an antigen.

252
Q

What does a type 1 immune reaction cause?

A

It causes either a local (hayfever) or systemic (anaphylaxis) reaction

253
Q

What is treatment for type 1 reactions?

A

Preventing exposure, anti-histamines and steroids

254
Q

What are type 2 reactions?

A

Immunoglobulins bound to surface antigens

255
Q

What are type 3 reactions?

A

Antibodies and targets circulate. Little lumps of antibody and target get deposited in the skin, lung etc. and activate immunity, resulting in tissue damage

256
Q

What are type 4 reactions?

A

Formation of granulomas, it is a slow process. They are walled off areas nailing nasty things in place. They are dependant on T cell activation. Granuloma of T cell and macrophages are illustrated in reactions to TB

257
Q

When is IgM made?

A

It is made at the beginning of the infection

258
Q

What is IgG?

A

It is a highly specific molecule targeting single ‘epitopes’.

259
Q

What does IgE do?

A

It is made to things we’re allergic to. It doesn’t really do anything. You can live perfectly well without it.

260
Q

What is the function of lung surfactant?

A

It decreases surface tension of fluid in the lung. It allows homogeneous aeration. It allows maintenance of functional residual capacity.

261
Q

What is lung surfactant?

A

It is a surface active phospholipid containing surfactant proteins.

262
Q

How is lung surfactant produced?

A

Produced by type 2 pneumocytes from 34 weeks and there is a dramatic increase 2 weeks prior to birth

263
Q

What accelerates the production of lung surfactant?

A

Steroids and adrenaline

264
Q

What does lung surfactant deficiency cause?

A

It causes non-compliant lungs

265
Q

How does the first breath happen?

A

Fluid is squeezed out of the lung by the birth process. The adrenaline from stress increases the surfactant release. Air is inhaled. Oxygen vasodilates the pulmonary arteries. The umbilical arteries and ductus arteriesus constrict

266
Q

How is elastic recoil altered with age?

A

Collagen and elastin fibres have more cross-linking and rupturing, decreasing SA by 1/3rd so there is loss of elastic recoil.

267
Q

How is gas exchange altered with age?

A

There is impaired gas exchange due to V/Q mismatch, reduction in alveolar SA, reduction in lung capillaries and reduction in blood flow

268
Q

How does oxygen saturation change with age?

A

Oxygen saturation decreases with age, it is not noticeable during daily activities and is only important during exercise.

269
Q

How does lung immunity change with age?

A

There is impaired immunity due to: decrease in glandular epithelial cells (less productive mucus); decrease in sputum clearance; small airways collapse and there is immunoscenesence.

270
Q

How does the chest wall change with age?

A

There are changes in the shape of the thorax, kyphosis (hunching) increases. The costal cartilages calcification and stiffness.

271
Q

How are muscle fibres altered with age?

A

There is a loss of fast type muscle fibres and a loss of total muscle mass in skeletal muscle (intercostals).

272
Q

How does the diaphragm muscle altered with age?

A

There is a decreased power of the diaphragm due to shape changes of the rib cage.

273
Q

How does diving affect the lungs?

A

Hydrostatic pressure means there is less blood in the limbs, so the thoracic blood volume increases, the CO increases, the vital capacity decreases, the lung compliance decreases so there are stiffer lungs, the residual volume increases.

274
Q

How does the depth of diving affect the lungs?

A

The increase of depth is proportional to the increase of gas density (pressure) which is proportional to the work needed to breath

275
Q

What is the normal response to lungs at altitude?

A

Hypoxia leads to hyperventilation (pH increases), which increases minute ventilation, lowers PaCO2, tachycardia and gets rid of renal bicarbonates.

276
Q

What are the high altitude illnesses?

A

Acute mountain sickness; high altitude pulmonary oedema; high altitude cerebral oedema

277
Q

How does acute mountain sickness work?

A

It is caused by recent ascent to over 2500m. The patient has a lake Louise score > 3. It causes headaches, dizziness confusion and vommitting

278
Q

How does high altitude pulmonary oedema work?

A

It is rapid ascent of over 8000ft. The symptoms are acute mountain sickness, cough and shortness of breath

279
Q

What are the symptoms of the high altitude cerebral oedema?

A

Confusion, behaviour change, acute mountain sickness is not a pre-requisite. It is serious

280
Q

What is Laplace’s law?

A

P = 2T/r

281
Q

How does Laplace’s law affect lungs?

A

The smaller airways get smaller because they need more pressure to open them.

282
Q

What is the function of the respiratory pump?

A

It is the generation of negative intra-alveolar pressure, inspiration is an active requirement to generate flow

283
Q

How does the bony thorax affect the respiratory pump?

A

The bony thorax structure is intimately linked to the function of the respiratory pump. It supports the respiratory muscles and protects the lungs

284
Q

Where does gas exchange take place?

A

In the alveoli and capillaries.

285
Q

How many capillaries are there per alveoli?

A

There are 1000 capillaries per alveolus. Each RBC could come into contact with multiple alveoli.

286
Q

At rest how long does it take to saturate a haemoglobin?

A

25% of the way through the capillary the haemoglobin is fully saturated.

287
Q

How much of the alveoli is used at rest?

A

30% of the total capacity is used at rest. Recruiting of the alveoli occurs at a consequence of exercise. Alveoli at the bases are preferentially ventilated at rest.

288
Q

What shape is the O2/Hb dissociation curve?

A

It is a non-linear sigmoid shape

289
Q

What affects the Hb affinity with oxygen?

A

CO, reduced temperature and H+ all affect the Hb affinity with oxygen

290
Q

How does CO affect the Hb affinity with oxygen?

A

It has 200 more times affinity for Hb than oxygen has, so the presence of CO also shifts the curve to left and there is a loss of sigmoid shape occurs.

291
Q

How do you work out the PAO2?

A

PAO2 = PiO2 - PaCO2/R

292
Q

What is the pH of ECF?

A

7.35-7.45

293
Q

Are the acids and bases of the body weak or strong?

A

They are weak. HCO3- is a weak base and H2CO3 is a weak acid

294
Q

What are the three main buffering systems of the body fluids?

A

(1) intracellular and extra cellular buffers (2) the lungs eliminating CO2 (3) renal HCO3- reabsorption and H+ elimination

295
Q

What is the main blood and tissue buffer?

A

HCO3- / H2CO3

296
Q

Is CO2 under respiratory or renal control?

A

Respiratory

297
Q

Is HCO3- under predominant renal or respiratory control?

A

Renal control

298
Q

How are fixed acids eliminated?

A

Through the renal system

299
Q

Are acids produced by metabolic processes volatile or non-volatile?

A

Acids continually produced by metabolic processes can be volatile (H2CO3) and non-volatile (sulfuric or hydrochloric)

300
Q

How are volatile acids different from non-volatile?

A

Non-volatile acids cannot be eliminated by the lungs, they are buffered by proteins or extracellular buffers then excreted normally by the renal system

301
Q

Where is lateral displacement of the lung by the heart on the left lung?

A

4-6th rib

302
Q

What leaves impressions on the right lung?

A

Azygos vein and the superior vena cava

303
Q

What leaves impressions on the left lung?

A

Heart and aortic arch

304
Q

What is the structure of the lung hilum vessels?

A

On both sides: the bronchus is posterior, and the pulmonary veins are anterior and inferior.

On the right side: the pulmonary arteries lie anterior to the bronchus.

On the left side: the arteries are the most superior vessel

305
Q

What happens to the thyroid gland during swallowing?

A

It is elevated

306
Q

Where does the superior thyroid artery come from?

A

The external carotid artery

307
Q

Where does the inferior thyroid artery come from?

A

The subclavian artery

308
Q

Try to learn this graph:

A

Cover up the right hand side and fill in the words

309
Q

What is the function of the residual volume?

A

Helps keep alveoli inflated between breaths

310
Q

In the fetal circulation are the umbilical artery and vein oxygenated or deoxygenated?

A

The umbilical vein is oxygenated.

The umbilical artery is mainly dexygenated.

The goal is to bypass the fetal lungs

311
Q

How does the fetal circulation bypass the lungs?

A

Foramen ovale (right ventricle -> left ventricle)

Ductus arteriosus anastamoses (pumonary artery -> proximal descending aorta)

Ductus venosus shunt (left umbilical vein -> IVC)

312
Q

Where is the oblique fissure?

A

Starts at T3 at the back, reaches the 6the rib laterall and follows the course of the 6th rib

313
Q

What is inside the anterior triangle of the neck?

A

Thyroid gland, carotid sheath, infrahyoid and suprahyoid muscles

314
Q

Why does the thyroid have a rich blood supply?

A

Deliver sufficient iodine

Rapid delivery of TSH

Rapid ‘washout’ of thyroxine

315
Q

What does the internal superior laryngeal nerve do?

A

Supplies sensation to the laryngopharynx

316
Q

What does the external superior laryngeal nerve do?

A

Supplies cricothyroid

317
Q

What does the recurrent laryngeal nerve do?

A

Supplies all laryngeal muscles other than the cricothyroid

318
Q
A

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