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Year 1 Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the most superior portion of the respiratory tract?

A

The nose/nasal cavity

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2
Q

What is the function of the nose/nasal cavity?

A

Increase the temperature of the air, increase the humidity, filter the air and take particles to be swallowed.

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3
Q

What is the inside of the nose like?

A

Initially skin with hairs in the vestibule then the SA is doubled by the turbinates which are inside.

Beneath the turbinates are the meatuses

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4
Q

Describe the Turbinates and area around them.

A

Turbinates - 3-4 bony shelves covered by erectile mucosa to increase the SA

Meatuses:

Superior meatus - Drains sphenoid and posterior ethmoid sinus

Middle meatus - Drains the frontal, anterior ethmoid and maxiallary sinus

Inferior Meatus - contains the orifice of the nasolacrimal duct

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5
Q

What are the names of the sinuses?

A

Frontal, Maxillary, ethmoid and sphenoid

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6
Q

Describe the frontal sinus

A

in frontal bone in midline septum over the orbit and across superciliary arch. innervated by opthalmic division of trigemina V

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7
Q

Describe the mailiary sinus

A

opens into the middle meatus through the semilunar hiatus

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8
Q

Ethmoid sinus describe it.

A

Labirynth of air pockets between the eyes

Anterior drains into the middle meatus through the ethmoid infundibulum

Posterior drains into the sphenoethmoidal recess in the superior meatus.

Innervated by the ophthalmic and maxillary branches of the trigeminal nerve

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9
Q

Describe the Sphenoid sinus

A

medial to the cavernous sinus
inferior to optic canal and pituitary gland
lateral to the nasal septum
it empties into the sphenoethmoidal recess in the superior meatus
innervated by ophthalmic division of the trigeminal nerve

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10
Q

what are the boundaries and sections of the pharynx

A

skull base to C6, split into nasopharynx oropharynx and laringopharynx

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11
Q

What happens in the nasopharynx

A

Eustachian tube enders with the ears

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12
Q

What are the names of the laryngeal cartilages?

A

Single- epiglottis, theyroid and cricoid
Double- Cuneiform Corniculate and Arytenoid

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13
Q

What is the innervation of the larynx?

A

The vagus supplies all of the innervation to the larynx
there are two branches the Superior laryngeal nerve and the recurrent laryngeal nerve.
The superior laryngeal provides sensory to above the glottis and the external branch does the motor innervation to cricothyroid.
the recurrent laryngeal nerve provides sensory innervation to the infra glottis, and motor innervation to all the internal muscles other than cricothyroid

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14
Q

Where is the Carina?

A

T4/5

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15
Q

What shape is the trachea?

A

Oval

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16
Q

What shape are tracheal cartilages?

A

Semicircular cartilages

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17
Q

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

A

the right is shorter 1-3cm long and more vertically disposed the left is less vertical and longer at 5cm

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18
Q

What is the lingular lobe?

A

probably reminant of left middle lobe

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19
Q

What are the names of the lobes of the lungs?

A

Right- upper, middle and lower

Left upper, and lower lobe (with linguilla)

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20
Q

What are the divisions of the lungs?

A

lungs lobes segments

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21
Q

Describe the pathway of the airways

A

Trachea, R/L main bronchus, lobar bronchi, segmental bronchi, terminal bronchiole(end of conduction), respiratory bronchioles alveolar duct alveoli.

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22
Q

What is the lung acinus?

A

Functional unit of the lung made of many small alveoli

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23
Q

What are the types of cells in the Alveoli?

A

Type 1 surface area, Type 2 surfactant, Alveolar macrophages basement membrane and capillary endothelial cells

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24
Q

What is difference of the visceral and parietal pleura?

A

Visceral adherent to the lungs, single cell layer has only autonomic(stretch) receptors
parietal is on walls has pain sensation

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25
Q

What is the bronchial circulation?

A

Bronchial circulation is the blood supply to the lung tissue and the pulmonary arteries follow the bronchi.

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26
Q

What is the rough volume of air through the lungs in a minute?

A

5litres

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27
Q

which nerve innervates the diaphragm?

A

the phrenic C3,4,5

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28
Q

What is the significance of the interpleural space?

A

has a few mililitres of fluidto lubricate its is a potential space

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29
Q

What is ventilation and perfusion?

A

ventilation is the movement of air in and out of the lung. perfusion is a blood supply to the area of the lung.

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30
Q

What is dead space?

A

volume of air not contributing to ventilation?

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31
Q

What are the divisions of dead space?

A

Anatomic 150mls and alveolar 25mls isn’t much blood there so physiological dead space is both 175ml

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32
Q

What can affect the perfusion of a lung?

A

pulmonary artery pressure, pulmonary venous pressure and alveolar pressure.

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33
Q

What is hypoxic pulmonary vasoconstriction?

A

when there are low levels of oxygen in the lung the vessels constrict

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34
Q

PaCO2, PACO2 Pi O2 mean what?

A

arterial CO2 alveolar CO2 pressure of inspired O2

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35
Q

VA VCO2 mean what?

A

alveolar ventilation and CO2 production

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36
Q

How is CO2 carried in the blood?

A

Dissolved in plasma, Attached to haemoglobin and as carbonic acid

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37
Q

What are physiological causes of high CO2?

A

reduced minute ventilation, shallow rapid breathing as lots is dead space, Vdot A reduced by increased dead space ventilation, Increased CO2 production

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38
Q

What is the alveolar gas equation?

A

PAO2=PiO2- PaCO2/Resp quotient.

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39
Q

What cause hypoxaemia low O2

A

Alveolar hypoventilation, reduced O2 pressure V/Q mismatch and diffusion abnormality.

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40
Q

What factors affect binding of Oxygen with Haemoglobin?

A

CO, 2,3 DPG, pH, temperature

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41
Q

What does carbonic anhydrase catalyse?

A

The joining of carbon dioxide and water.

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42
Q

What are the non immune defences of the lung?

A

Epithelium

Nasal Hairs

Mucous

Mucociliary escalator

Cough

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43
Q

What are the clinical features of inflamation?

A

Calor (heat) Rubor (redness) Dolor (pain) Tumour (swelling) Functio laesa (loss of function)

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44
Q

What are the physiological inflamatory features?

A

Vasodilatation leadint to more plasma exudation, activation of biochemical cascades, migration of leukocytes into the tissues such as neutropils and monocytes

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45
Q

What is the double edged sword in body’s response to disease?

A

Inflamation fights infection but lots of people will die from inflamation.

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46
Q

What is the cause of COPD?

A

smoking fossil fuels etc but due to inflamation in the lungs

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47
Q

What is ARDS?

A

Acute Respiratory Distress Syndrome

Respiratory failure, water and neurtrophils fill the alveoli is part of multi-system failure. untreatble but supportive care. there is endothelial leak leadind to stiff lungs, there is shunting v/Q mismatch, the pulmonary constricution reduced cardiac output

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48
Q

Adaptive immune cells are made where?

A

in the bone marrow

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49
Q

What is the original cell of the blood cells?

A

haematopoeitic stem cells.

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50
Q

What percentage of wbc are neutrophils?

A

70%80 millin are made each minute. they contain granules wich release myeloperoxidates elastase or secondary receptors lysoszyme and collagenase

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51
Q

How can neutrophils be turned off?

A

macrophages can absorb neutrophils

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52
Q

what are the roles of neutrophils?

A

activation after identification, adhesion, migration/chemotaxis, phagocytosis, bacterial killing

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53
Q

What do neutrophil receptors recognise?

A

PAMPs and DAMPs

recognise cell walls lipids and peptides of bacteriahost mediator cytokines host opsonins like immunoglobulins. and adhesion molecules

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54
Q

Describe neutrophil activation

A

stimulus response coupling, signal transduction pathways and release granules

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55
Q

Describe neutrophil adhesion

A

margination- Neutrophil activation by selectins and chemokines regulates integrin adhesiveness. Binding of activated integrins to their counter-receptors on endothelial cells induces neutrophil arrest and firm adhesion.

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56
Q

Describe neutrophil migration

A

ability to dectect concentration gradient and move along the gradient

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57
Q

Describe phagocytosis

A

invagination called phagoome, and granules joing called a phagolysosome

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58
Q

Describe neutrophil bacteral killing

A

lysosomal enzymes elastase and reactive oxygen species. ROS generated there are many and genetic prolems can affect.

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59
Q

What is airway tone?

A

the contraction or relaxation of muscle in the airways.

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60
Q

What are some differences between asthma and COPD?

A

Asthma- usually younger than 50 not linked to smoking, infrequent sputum, lots of allergies, stable with exacerbations, normalise spiromitry with treatment, intrmittent symptoms, responds to treatment.

COPD- Usually older than 35, 10 pack year, comon in chronic bronchitis, no link with allergies, progressive with exacerbations, unlikely to improve persistent symptoms, doesn’t respond well to treatment there is a lot of asthma

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61
Q

What regulates the airways smooth muscle tone?

A

the autonomic nervous system and is regulated by inflamation.

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62
Q

Describe the effect of the parasympathetic nervous system on the airways

A

it causes bromchoconstriction the vagus nerve does this, they release acetyl choline which acts on muscarinic receptors(M3) in muscle cells.

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63
Q

How can excessive bronchoconstriction be treated?

A

You use drugs that inhibit/ block the M3 receptor called anti-cholinergics or anti-muscarinics

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64
Q

What are SAMAs?

A

Short acting muscarinic antagonists. They include ipratropium bromide (Atrovent) which can be used as inhaled treatment to relax airways they arent used too often as long acting are bettter, are uses in acute management

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65
Q

What is a LAMA?

A

long acting muscarinic antagonist. They have a long duration of many hours such as tiotropium they increase bronchodilation. they seem to reduce acute attacks they also affect the mucus production

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66
Q

What is the effect of the sympathetic nervous system on the airways?

A

Release noradrenaline with activates adrenergic receptors there are alpha and beta. in humans they mainly do blood vessels but also do the smooth muscle beta 2 receptor acivation causes relaxation of smooth muscle

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67
Q

What is a SABA?

A

Short acting beta2 agonists such as salbutamol.

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68
Q

What is a LABA?

A

Long acting beta 2 agonist like salmeterol or formoterol.

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69
Q

How are SABA/LABAs given for asthma?

A

With steroids, uses in acute rescue of bronchoconstriction and to prevent bronchoconstriction which reduces rates of exacerbations

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70
Q

What are the adverse effects of Beta2 agonists?

A

drives potassium into the cells so causes low levels in the blood, it can increase the heart rate. can cause hyperglycaemia.

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71
Q

What is the main factor the governs drug deposition and other factors?

A

particle size makes a difference. The device(dry powder inhalter or mdi) the flow rate of inhalation, underlying disease or regional differences in lung ventilation

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72
Q

What is important about asthma treatment?

A

concordance is low, inhaler education is key and correct device selection is vital

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73
Q

What are the goals of asthma treatment?

A

Get control of symptoms, relief of symptoms

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74
Q

What are the immeiate management of asthma?

A

Oxygen up to 60%, Salbutamol nebuliser prednisolone(steroid tablet), give magnesium or aminiphylline IV

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75
Q

What are the functions of the lungs?

A

Oxygenation of blood, release of carbon dioxide, synthesis activation and inactivation of vasoactive substances, hormones, neuropeptides, lung defence speech vomiting defecation childbirth

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76
Q

What are the three levels of defence in the lung?

A

intrinsic, innate, and adaptive

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77
Q

What are some of the nonspecfic defence mechanisms in the respiratory system.

A

Anti-proteases lysoszomes phospholipase A, Anti fugal peptides ant microbial peptides, surfactant that can opsonize pathogens for phagocytosis. there are also non-pathogenic bacteria.

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78
Q

What is the biggest defence in the lungs?

A

mucus production and release with cilliary escalator

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79
Q

What is the host defence in the alveolar gas exchange?

A

surfactant and a physical barrier

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80
Q

What is pericilliary fluid?

A

the fluid around the cilia wafts the fluid and the mucous moves over the top.

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81
Q

What is coughing?

A

reflext to expell foreign bodies, or an irritating particulate. can be volunatry and involuntary

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82
Q

What is sneezing?

A

it is an involuntary expulsion of nasal irritation. from pollen smoke or too much fluid.

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83
Q

How do cells come back after dammage?

A

spreading and dedifferentiation and then cell migration and proliferation and re differentiation but doesn’t get fully better. this is functional plasticity

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84
Q

what happens if a bronchiole is blocked?

A

the gas exchange is blocked, then bacteria and bad can’t get out causes infection.

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85
Q

What can cause a mucus plug?

A

goblet cell metaplasia where there are too many goblet cells due to tissue damage.

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86
Q

What are the named volumes on a analysis graph that you might have?

A

Total lung capacity, vital capacity, residual volume, inspiratory reserve volume, expiratory reserve volume, forced tidal volume, functional residual capacity, inspiratory capacity.

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87
Q

What are other measured values?

A

FEV1 forced expiratory volume in one second, FVC forced vital capacity, peak expiratory flow, lung volumes transfer factor estimates

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88
Q

What is the difference between volume time and flow volume plots?

A

volume time is steep curve to plateau. flow volume is a steep upward curve then slower plateau to 0 flow after. in normal person it should be a straight line after PEF has been reached.

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89
Q

What are important things to note on flow/volume plot?

A

Peak flow is top point, FEF is the flow at when 25% has been exhaled.

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90
Q

What are the units for peak flow?

A

L/min. can use a peak flow or spirometer. they need to blow very hard! (effort dependent)

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91
Q

What are the problems with measuring the total lung capacity?

A

can’t expel all the air in the lungs only the forced vital capacity.

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92
Q

What methods can be used to measure total lung volume?

A

Gas dilution- doesn’t measure the air in communicating bullae

closed-circuit helium or open circuit nitrogen washout. A known amount of helium is added and when you breathe out we measure the new concentration and from that can work out the volume in the lungs

Body box or plethysmography- can measure gas in bullae, patient pants with open glottis against a shutter to produce changes in the pressure of the box in proportion to the volume of air in the chest.

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93
Q

How can we estimate transfer rates?

A

Using carbon monoxide to estimate DL CO wich is a measure of interaction of alveolar surface area alveolar capillary perusion capillary volume and haemoglobin concentration. need 10 second breath hold.

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94
Q

What is a low FEV1?

A

Anything about 80% or greater of you predicted value.

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95
Q

What is it called when FVC is lower than 80% of predicted value?

A

Airways restriction.

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96
Q

What is FEV1/FVC when its lower called?

A

less than 0.7 is airways obstruction this reduces with age.

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97
Q

What does an asthmatic flow volume loop look like?

A

the lower one is scalloped and the FEV1 is lower

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98
Q

What are the blood gases in acute asthma?

A

PaO2 normal, Pa CO2 low,pH normal or elevated,HCO3 normal

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99
Q

What are the flow loop for a COPD patient?

A

scalloped and lower PEF.

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100
Q

What are the test results of asthma?

A

Airways obstruction and PEF variation but variable problems. normal or reduced FEV1 normal FVC, PEF usually lower at times, MEF scalloped TLC high or normal, normal DLco

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101
Q

What are the symptoms of COPD?

A

FEV1 reduced significantly, FVC may be normal or reduced, PEF not variable, MEF low scalloped shape, Low transfer rates.

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102
Q

What is dynamic hyperinflation?

A

refers to the increase in end-expiratory lung volume (EELV) that may occur in patients with airflow limitation when minute ventilation increases. pasically tidal levels increased

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103
Q

What is COPD blood gas like?

A

low PaO2 High Pa CO2 in type 2 low in type 1 pH normal may have elevated HCO3 if chronic acidosis is present.

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104
Q

What are test results of pulmonary fibrosis?

A

Reduced significanly reduced FEV1 FVC. stable PEF low or normal MEF, TLC reduced low transfer measures normal eNO.

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105
Q

Blood gasses for pulmonary fibrosis?

A

PaO2 is low, Pa CO2 low, pH normal, HCO3 low.

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106
Q

What causes the urge to breath?

A

Carbon dioxide sensors in health

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107
Q

What is a normal respiratory rate?

A

12-20 breaths per minute

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108
Q

What proportion of blood goes through the bronchial circulation?

A

2%

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109
Q

What is the surface area of gas exchange roughly?

A

50-100m^2

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110
Q

What are the differences between the systemic system and pulmonary vasculature in the lungs?

A

Thin walls in pulmonary thick in systemic

highly muscularised in systemic less so in pulmonary

lots of redistribution in systemic and pulmonary not as much.

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111
Q

What is Pousieuille’s Law?

A

Resistance = 8xLxviscocity/Pi r^4 so the bigger the radius of the vessel the less the resistance.

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112
Q

What happens to to reduce resistance in the lungs?

A

Recruitment with more blood vessels and the vessels can distend this can maintain pressure when then cardiac output is increased.

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113
Q

What is hypoxaemia?

A

The lack of sufficient oxygen in the blood

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114
Q

What are the two types of respiratory failure defined as?

A

Type 1 pO2 is below 8kPA pCO2 is less than 6kPAType 2 pO2 is below 8kPA pCO2 is above 6kPA

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115
Q

What are the main causes of hypoxaemia?

A

Hypoventilation, Diffusion impairment, Shunting, V/Q mismatch

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116
Q

What is usually the cause of type 2 respiratory failure?

A

Hypoventilation which can be due to muscular weakness, Obesity, Loss of respiratory drive.

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117
Q

What is diffusion impairment?

A

When the gases struggle to pass across the membrane.. Pulmonary oedema, anaemia, interstitial fibrosis

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118
Q

What is V/Q mismatch in a normal Physiological lung?

A

top of lung has no blood flow, middle arterial is greater than alveolar so some blood flow happens. the bottom the alveolar pressure is much higher.blood flow is higher at the top high VQ bottom low VQ

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119
Q

What is a shunt?

A

when there is a blockage to an airway or artery causing a v/Q mismatch.

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120
Q

What are causes of shunts?

A

Bronchial artery blockage Ventricular septal defect, Arterio venous malformation and lobar collapse

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121
Q

What is hypoxic pulmonary vasoconstriction?

A

When there is low oxygen in the lung the blood vessels constrict.

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122
Q

what are diseases of pulmonary circulation.

A

Pulmonary embolism, pulmonary hypertention pulmonary AVM

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123
Q

Where does the lung develop from?

A

the foregut ventral outpouching in the 5th week

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124
Q

What happens between 5-17 weeks in the lungs?

A

major exocrine gland, major structural units formed, angiogenesis lung fluid is looking like a secretory gland

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125
Q

What happens after 17 weeks to 25 weeks?

A

Canalicular phase, there is development of the distal architechture and the blood vessels form capillary bed.

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126
Q

What happens upto birth?

A

get alveolar sacs develop two types for cells.

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127
Q

when does lung development stop?

A

At about 5 years old

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128
Q

What can go wrong in embryonic stage of lung development?

A

fistula between trachea and oesophagus, lung dvelopment of one lung due to stenosis

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129
Q

What can go wrong in canalicular stage?

A

if blood supply doesn’t develop well, also problems with alveolus and capillary. acinar prolems

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130
Q

What is the most common problem in premature babies in terms of lung development?

A

the alveolus is not properly developed and doesn’t function very well

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131
Q

What is oxygen in the pulmonary circulation?

A

it is a vasodilator and so in lungs blood chases oxygen.

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132
Q

What happens in foetal lungs?

A

not good for oxygenation so have shunts in ductus arteriosis and shunting in atria. blood flows to the plcenta not lungs because there is high resistance from the lungs

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133
Q

What is 123 in foetal circulation?

A

1 unmbilical vein caries the oxygenated blood to the liver. 2 umbilical arteries come from illiac area to the placenta. 3 shunts exist, ductus venousus in the hepatic to allow blood to the IVC, foramen ovale between left and right atria and Ductus arterosus a ein connecting the pulmonary artery to descending aorta

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134
Q

What happens after birth?

A

oxygen comes into the lungs and perfusion begins in the lungs. the shunts close up due to pressures. after birth the PA presssure is lower than the Aorta.

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135
Q

What can go wrong after baby is born?

A

persistent pulmonary hypertension of newborn as the lungs are not allowing the blood coming into the lungs. the pressure in lungs has not been reduced

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136
Q

What happens in the alveolus after birth?

A

After birth the lungs begin to absorb the fluid very quickly to allow for gas exchange. this switch is from a secretory channel.

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137
Q

What is Laplace’s law?

A

Pressure= 2T/radius

more pressure required to inflate a small sphere. surface tension tries to colapse the lungs the surfactant changes this.

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138
Q

What is surfactant?

A

it reduces surface tension phosphilipid secretion fromt he lungs it is made of proteins as well. produced by type 2 pneumocytes. ti reduces surface tension allowing them to expand homogenously.

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139
Q

What are problems relating to surfactants?

A

Prematurity the cells aren’t very good at producing it especially if cold or ypoxic. Respiratory distress syndrome can develop. the can have non-compliant lungs.

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140
Q

What is the name of the classification system of immune responses?

A

Gel and coumbs

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141
Q

What are cytokines?

A

Proteins that allow leukocytes and tissue cells to talk to eachother

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142
Q

Where do antigen presenting cells go?

A

to the lymph nodes

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143
Q

When are IgM antibodies made?

A

at the beginning of an infection

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144
Q

What are IgG?

A

highly specific that targed specific epitopes

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145
Q

What are Ig E?

A

Made to things we are allergic to and could be involved in response to parasites.

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146
Q

Where can IgA be found?

A

It can be found in mucous membranes

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147
Q

Outline the Gell and coombs classifications

A

Type 1- IgE acute anaphylaxis, hay fever

Type 2 Ig bound to cell surface antigens, Transfusion rections autoimmune diseases

Type 3 Immune complexes, activation of complement SLE, post-streptococcal GN

Type 4 T cell mediated DTH TB contact dermatitis

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148
Q

Describe Type 1 reactions immune

A

Immunological memory to something causing an allergic response. Acute anaphalaxis, hayfevere and asthma

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149
Q

What is Atopy?

A

inherited tendency to exaggerated IgE response to an antigen.

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150
Q

What is anaphalaxis usually linked with?

A

IgE and histamine attaching to mast cells

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151
Q

How is atopy diagnosed?

A

Skin prick tests, RAST radio

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152
Q

What is goodpasture’s syndrome?

A

A type 2 teactio where there are antibodies to basement membranes. Follows a viral infection sometimes. teatment to remove antibodies.

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153
Q

What are some common drug causes of hypersensitivity

A

Nitrofurantoin, Aminodarone, bleomycin, methotrexate, NSAIDs Immunoglobulin based treatements

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154
Q

What are some common lung diseases that are genetically linked?

A

Cystic fibrosis, Alpha-1 antitrypsin deficiency

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155
Q

How do genetics and disease presentation link?

A

Rare alleles caue the most sever disease more common cause things like COPD

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156
Q

at what age is it likelt that your lungs stop growing?

A

around 19/20 steepest growth is after 10 years

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157
Q

At what age is it expected that lung function peaks?

A

At around 20-25 years old

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158
Q

What is Cystic fibrosis?

A

chroic genetic disease which can involve many organs abour 10,000 affected UK, Frequent chest infections malabsorptio failure to thrive abnormal salt chloride exchange can lead to infertility.

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159
Q

Describe the genetics of Cystic fibrosis.

A

most common lethal autosomal recessive genetic disorder in caucasions, Chromosome 7 defect in CFTR protein, 1600 mutations associated.

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160
Q

What does the CFTR protein do?

A

It transports chloride ions out of the cell. this helps with epithelial fluid managment includes lung and GI usually

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161
Q

What does the treatment of CF include?

A

Rescue when exacerbations occur, prevention or maintenance treatment

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162
Q

Explain rescue care in CF

A

2 week iv antibiotics can be done at home or hospital but can cause allergies renal impairment resistance and vein access problems

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163
Q

What does CF prevention management include?

A

Segregation to avoid infection, Surveillace every 3 months, airway clearance using physio, nutritional support such as enzymes high calorie and fat and suppliments, phsycological support.Antibiotic nebulisers can be used, inhalors steroids, vaccinations can also be used

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164
Q

What are/could be the applications of personalised medicine for CF

A

The fact one specific gene is affected is important and helpful. it has clear therapeutic targets and there can be directed genotype therapies developed.

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165
Q

What are some of the genotype directed therapies of CF?

A

Small molecule ganets facilitate CFTR processing (Ivacaftor) Orkambi mixed outcomes gene therapy nees more work on delivery of the drug

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166
Q

What is alpha-1 antitrypsin deficiency?

A

an autosomal recessive genetic disorder, There are 80 different mutations in the gene in Chromosome 14 it causes early onsed emphysema and bromchiectasis as the elastase in the lung is broken down.

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167
Q

Why is PaCO2 more important?

A

can change the pH of the blood which is not really wanted.

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168
Q

Which are the inputs to the brain involved with breathing?

A

Central chemo receptors in the brainstem, voluntary input from the cerebrum, lung stretch receptors, J receptors and irritants (mechno receptors). peripheral chemo receptors in the carotid and aortic, muscle proprioceptors all feed to the medulla and pons.

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169
Q

What are the areas of the brainstem that are involved with respiratory control?

A

pneumotaxic and apneustic centres in the pons, dorsal and ventral respiratory group in the medulla.

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170
Q

What do the Pneumotaxic and apneustic centre do?

A

it slows down or inhibits inspiration. and the apneustic moderates the pneumotaxic

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171
Q

What is the function of the dorsal and ventral respiratory groups?

A

dorsal is mainly active in inspiration. ventral is uses in both inspiration and expiration.

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172
Q

What is the central pattern generator?

A

It is located withing DRV VRG it starts and stops and resets the ventilatory drive.

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173
Q

What percentage of influence in central and peripheral does PaCO2 have?

A

central 60%, peripheral40%.

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174
Q

What is the primary influence in central chemo receptors?

A

PaCO2in carotids it is PaCO2 and PaO2 and pH.

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175
Q

Where are the central chemoreceptors?

A

in the pontomedullary junction.

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176
Q

Why are central chemoreceptors more sensitive to PaCO2 than H+

A

Hydrogen ions cannot pass across theblood brain barrier . whereas CO2 can

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177
Q

In the brain how are CO2 levels sensed?

A

By the H+ concentration from carbonic anhydrase,

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178
Q

Where are the carotid and aortic bodies?

A

bifurcation of common carotid, IX cranial nerve afferents, asending aorta and has vagal nerve afferents.

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179
Q

Whats the main sensor of oxygen?

A

the peripheral chemoreceptors not active across all PaO2 type 1 can release neurotransmitter when hypoxia.

180
Q

What do stretch receptors do in the lung?

A

Sense lung volume for slowly adapting and fast adapting the smooth muscle of conducting airways.

181
Q

What are irritant receptors like?

A

irritant receptors are in conducting airways and do gasp or cough reception,

182
Q

What are J receptors?

A

Juxtapulmonary capillary the have C fibres

183
Q

Where are some other receptors?

A

Nose nasopharynx and larynx. There are chemo and mechano receptors.

184
Q

what are the muscle proprioceptors?

A

In the joints tendons and muscle spindle receptors in the intercostal muscles and the diaphragm.

185
Q

What happens as you walk up a mountain?

A

PiO2 is reduced Fraction of O2 staysthe same. then alveolare oxygen reduces so arterial oxygen drops and therefor ventilation is increased.

186
Q

What does ACID stand for and mean?

A

Gell and coombs
A – allergic
C – cytotoxic killing
I – immune complexes
D – delayed T helper cells

187
Q

What happens in oxygen content of air in height?

A

the pecentage stays the same, but the pressure of oxygen would be lower in proportion to others.

188
Q

What is intersting about oxygen pressure changes?

A

It changes the saturation of haemoglobin but not in a linear way.

189
Q

What happens to body at high altitude?

A

Increased ventilation, lowers PaCO2 alkalotic and get thachycardia, with time this is reduce and the alkalosis is compensated by renal bicarbonate.

190
Q

What are the three common altitude problems?

A

Acute mountain sickness, High altitude pulmonary Oedema and High altitude Cerebral Oedema.

191
Q

What is Acute mountain sickness?

A

Lake louise score >= 3 have a headache and one other symptom recent ascent to over 2500m only reliable treatment is descend, and have O2 recompress acetoazolamide. younger people are more likely to have it.

192
Q

What is the cause of high altitude pulmonary oedema?

A

An increase in altitude results in a decrease in piO2 which therefore means more of the alveoli become hypoxic and as a result, there is increased pulmonary vessel vasoconstriction which increases pulmonary pressure. this forces more fluid out of the blood vessels and into the interstitial space causing oedema.

193
Q

What is high altitude cerebreal oedema?

A

Serious Confusion behaviour change,

With Immediate descent, symptoms can resolve relatively quickly.

194
Q

What can be done for people flying?

A

give oxygen

195
Q

What is 10m of sea water equivalent to in pressure?

A

10m= 1ATM

196
Q

What is boyles law?

A

P1V1=P2V1 when you change the volume the pressure changes and when you change the pressure the volume changes.

197
Q

what happened in apnoea diving?(breath hold)

A

Hyperventilate, descend holding breath. PaO2 PaN2 and PaCO2 increase as pressure in lungs increase. Minimal N2 absorption normally Taravana is going mad from it. CO2 builds u to induce desire. diver returns and levels fall again.

198
Q

What is shallow water death?

A

You dive for long time with low PaCO2 but lots of oxygen is used up and no response to make you take a breath

199
Q

What is the diving reflex?

A

stop breathing, bradycardia and peripheral vasoconstriction happens when cold water goes on the face

200
Q

What does SCUBA stand for?

A

Self-contained underwater breathing apparatus.

201
Q

What has to be considered with the gas canisters?

A

what ambient pressure you will be breathing the gas at.

202
Q

What is Dalton’s Law?

A

Each gas’s partial pressure adds to the total pressure.

203
Q

What is pulmonary oxygen toxicity?

A

Lorrain smith effect. any pressure of oxygen higher than 0.5 Atm. get symptoms in 12-24 hours. symptoms are cough chest tightness chest pain and shortness of breath. can happen in intensive care.

204
Q

How can you assess CNS oxygen toxicity?

A

VENTID

Vision

Ears(tinitus)

Nausea

Twitching

Irritability

Dizziness

Convulsions

205
Q

What is inert gas narcosis?

A

When a large amound of inert gas goes into all organs and happens at low depth, there is a lot of variation, there are other influencing factors, can be to do with lipid solubility.

206
Q

What is decompression illness?

A

N2 is usually poorly soluble but at depth, there is increased solubility due to henrys law

as you rise from the depths the pressure decreases and this causes bubbles of nitrogen to form in the blood and body tissues which can result in decompression sickness

207
Q

What is an arterial gas embolism?

A

Gas enters the circulation via a torn pulmonary vein. small pressure can can lead to arterial gas embolysm need recompression

208
Q

What is pulmonary barotrauma?

A

Barotrauma is tissue injury caused by a pressure-related change in body compartment gas volume.

alveolar rupture due to elevated trans alveolar pressure

air leaks into extra-alveolar tissue (leaks into the pleura) resulting in conditions including pneumothorax, pneumomediastinum

209
Q

What can cause lung problems?

A

Allergens Infection.

210
Q

What is asthma?

A

Chronic inflamatory disease inflamationin the airways.

211
Q

What are causes of asthma?

A

Environmental influences are important- pollens infectious agents fungi pets

Occupational- flour car spray paint resins cleaning agents laboratory animal workers wood dust.

212
Q

What is the epedemiology of asthma?

A

5-16% have it wide variation between countries. Increased prevalence second half of 20th centurey often found in poorer individuals.

213
Q

What is hypersensitivity pneumonitis?

A

Acute sub acute and chronic forms, immue complex related disease It is inflamation of the lung. IgG mediated significant environmental influences.

214
Q

What are occupational causes of COPD?

A

Silica Coal Grain Cotton Cadmium less common PAH Isocyanates steel/iron processing. Agricultural dust, Biomass fuels. wood dust

215
Q

What is the initial innate immune response to pathogens?

A

lt reacts quickly but in the same way each time

216
Q

What is the adaptive immune response like?

A

It reacts slowly on first infection but due to its memory it can react to secondary infections faster

217
Q

What is an antigen?

A

Any molecule that can induce a soecific immune response on the part of the host organism. it can be polysaccharide, lipids, DNA it can be soluble or part of the organism iself.

218
Q

Which cells are antigen presenting cells?

A

Dendritic and monocyte/ macrophages. when they meet a foreign molecule they ingest it and digest then display these cells on its surface.

219
Q

What are the two types of lymphocytes and what do they do?

A

T cells- secret cytokines, cytotoxicity and regulate immunity

B cells- release antibodies(immunoglobulins)

220
Q

What are the properties of adaptive immunity?

A

Ability to mount highly specific responses to a range of antigens, self-tolerance, and developing some form of a memory

221
Q

how do lymphocytes recognise specific antigens?

A

T and B cells have different unique antigen receptors. B cells use antibodies and Tcells receptors are similar.The diversity arises from different rearangements called VDJ variations.

222
Q

What is VDJ variety

A

During developement all but one V D and J versions are deleted and put into the RNA that forms many combinations.

223
Q

What happens when an antigen recognised?

A

There is prolieration of that cell and this is very prone to mutation which allows more varaiability and this allows for evolution.

224
Q

What is tolerance in immuity?

A

It is a state of unresponsiveness of the immune systen to antigens that would normally elicit an adaptive immune response.

225
Q

Why is tolerance to self needed?

A

To stop auto immune responses being devloped and in pregnancy.

226
Q

What is central tolerance?

A

It arises early in development where specials cells express all the antigens. T and B cells that react with these cells are colonially deleted or they develop into supressor cells this is common in T cells called Tregs they migrate into lymphoid tissue.

227
Q

What is peripheral tolerance?

A

when Tregs in lymphoid tissue suppress or delete lymphocytes that recognise the self antigens as foreign

228
Q

How is immunological memory developed?

A

Following activation of T or B cells they proliferate and some differentiate intolong-term memory cells that reside in tissue or lymph nodes. they are different becuase they have an increased lifespan and stronger affinity to antigens

229
Q

How are antigen presenting cells not phagoytosed themselves?

A

they display the antigen with major histocompatibility complex that shows that the cell is self (Human leukocyte antigen)

230
Q

What happens if a nieve cytotoxic cell meets an antigen presenting cell?

A

CD8+ it is stimulated to become a cytotoxic T cell it looks for cells with target antigen. if it finds one it binds to the cell and releases its granules.

231
Q

What happens when a helper T cell meets an antigen presenting cell?

A

CD4+ it can either release cytokines and can differentiate to different T helper cells, these include ones that activate macrophages ones that stimulate antibody production activate neutrophils pr provide long term immunity.

232
Q

How does a B cell begin its role?

A

The B cell is stimulated by an antigen. it differentiates to a plasma cell and memory cells, it releases antibodies with the same shape as its own.

233
Q

What is an IgM ?

A

immature plasma cells secrete it and happens in early response. the constant regions are not very available.

234
Q

What do IgA do?

A

dimer that can accesss mucosal surfaces and mediates mucosal immunity

235
Q

What to IgG and IgE do?

A

IgG are in circulation and activate phagocytosis, IgE bind to mast cells and mediates allergic reactions.

236
Q

What are some of the effects of antibodies?

A

Neutralisation, agglutination(joining together), opsonization allowing phagocytosis, complement fixation constant and directly kills it

237
Q

How is the immune response harnessed in vaccinations?

A

They stimulate the body to produce a response without the exposure to the pathogen.

238
Q

What happens with reduced b cell function?

A

failure to eliminate pathogens such as bacteria specifically ones which have a waxy capsule. this recurrent infecion can cause scars in the lungs

239
Q

What happens with failure of T cell immunity?

A

Primary is quite rare but HIV is secondary that are more common. Thisleads to opportunistic infections like TB Fungi Virus EBV CMV and parasites and some cancers

240
Q

How does HIV act?

A

It infects T helper cells CD4+ is specific on them. It leades to death ot T helper cells to reduce. there is a treatment to it in the form of retroviral drugs.

241
Q

What happens in failed tolerance?

A

Happens with age, there is a genetic ling and are more common in women. a cell escapes from the control and the body attacks itself by production of autoantibodies.

242
Q

What is rheumatoid arthritis?

A

Autoantibodies for molecules in joint tissues especally synovium. smoking can modify proteins seen in the lungs to the same as the synovium and cause disease

243
Q

What is ANCA vasulitis?

A

when anti-neutrophil cytoplasmic antibodies attach neutrophils and cause them to attack the body. This can affect the lung and the kidney causing inflammation

244
Q

How does chronic inflammation occur?

A

When infections persist or irritants or foreign bodies, there is an innapropriate response to the problem, it can occur when structural dammage is sustained

245
Q

What are the three patterns of chronic inflamation?

A

Suppurative inflammation where the cells are surrounded by a capsule of inflammatory cells or fibrous tissue

autoimmune inflammation can lead to fibrosis

granulomatous cells can lead to fibrosis as well.

246
Q

Example of suppurative infalmation

A

lung abscesses , could be caused by and organism could be caused by obstruction tissue damage or be impaired immune system

247
Q

What happens to rheumatoid dammage in thelung?

A

Repeated endothelial injury and leads to laying down of collagen and stops diffusion of oxygen, and leads to breathlessness

248
Q

What is granulomatous inflamation?

A

Caused by infections, inhaled antigens, aberrrant inflamation most common has unknown origin. a granuloma is a small nodule of organised collectons of macrophages called epitheliod and giant cells, surrounded by dense collection of lymphocytes and fibroblasts

249
Q

What are the consequences of chronic inflamation?

A

Systemic problems

malais

weight loss

fever

anaemia

Tissue destruction

cavity formation

Fibrosis

growth disorders like cancers.

250
Q

What is the treatment for chronic inflamation.

A

Treat the cause like infection or obstruction and immunosupressant drugs or NSAIDs

251
Q

What does the parasympathetic nervous system do to the lungs?

A

Constricts bronchi

252
Q

What does the sympathetic nervous system do to the lungs?

A

It dilates the bronchi

253
Q

What causes bronchoconstriction?

A

Parasympathetic nervous sytem

254
Q

What neurotransmitters are involved with bronchoconstriction/

A

Acetyl choline at both synapses

255
Q

What receptor causes bronchoconstriction?

A

ACh acting on M3 muscarinic receptors

256
Q

What are the treatments for bronchoconstriction?

A

Anticholinergic, muscarinic antagonists

257
Q

What receptor mediates smooth muscle relaxation?

A

Beta 2 adrenergic receptors

258
Q

What is released in the sympathetic nervous system to mediate bronchodilation?

A

Noradrenaline

259
Q

What are the types of adrenergic receptors?

A

Alpha and Beta,

260
Q

What structures contribute to the respiratory pump?

A

Bones (ribs and sternum), muscles (diaphragm and intercostals), pleura, nerves.

261
Q

What structures make up the conducting airways?

A

Nose, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles.

262
Q

What is the function of the conducting airways?

A

To filter, warm, humidify and conduct air to the lungs.

263
Q

What is respiratory epithelium?

A

Pseudo-stratified, columnar, ciliated, interspersed with goblet cells.

264
Q

Where is the resistance greatest in the airway?

A

In the trachea - the trachea is longer (length adds resistance) and there is only one of it (branching decreases resistance).

265
Q

What equation can be used to demonstrate resistance of an airway?

A

Poiseuille’s law: R = 8ƞl / πr^4.(ƞ = viscosity, l = length).

266
Q

Briefly describe inspiration.

A

Inspiration is an active process. The external intercostal muscles and diaphragm contract. The volume of the thoracic cavity increases and you get a negative intra-thoracic pressure; air is drawn in.

267
Q

What is the ‘pump handle’ representing?

A

The movement of the sternum. In inspiration the sternum moves anteriorly and superiorly.

268
Q

What is the ‘bucket handle’ representing?

A

The movement of the rib cage. In inspiration the rib cage moves upwards and outwards.

269
Q

Briefly describe expiration.

A

Expiration is usually passive. The ribs move down and in, the diaphragm relaxes. The intra-thoracic volume decreases and the pressure increases. Air is forced out.

270
Q

Which muscles are involved in active expiration?

A

The internal intercostals; these muscles contract pulling the ribcage inwards and downwards.

271
Q

What is V/Q mismatch?

A

When the perfusion of blood in capillaries isn’t matching the ventilation of the alveoli.

272
Q

What is it called when you have a high V/Q ratio?

A

Dead space. Lots of ventilation but no perfusion.

273
Q

What is a cause of a high V/Q ratio (dead space)?

A

Pulmonary embolism.

274
Q

What is it called when you have a low V/Q ratio?

A

Shunt. Lots of perfusion but no ventilation.

275
Q

What is a cause of a low V/Q ratio (shunt)?

A

Pulmonary oedema.

276
Q

What is perfusion of pulmonary capillaries dependent on?

A
  1. Pulmonary artery pressure.2. Pulmonary venous pressure.3. Alveolar pressure.
277
Q

Does the apex of the lung have a high or a low V/Q? Why?

A

High - effect of gravity, far more perfusion at the base of the lung.

278
Q

What are the 7 layers for gas exchange?

A
  1. Alveolar epithelium. 2. Interstitial fluid.3. Capillary endothelium.4. Plasma layer.5. RBC membrane.6. RBC cytoplasm.7. Hb binding sites.
279
Q

Name 4 causes of hypoxia.

A
  1. Hypoventilation.2. V/Q mismatch.3. Diffusion abnormality.4. Reduced PiO2.
280
Q

Name 4 causes of hypercapnia.

A
  1. Increased dead space ventilation; rapid, shallow breathing. 2. V/Q mismatch.3. Increased CO2 production.4. Reduced minute ventilation.
281
Q

What is the alveolar gas equation?

A

PAO2 = PiO2 - (PaCO2/R)

282
Q

What is Dalton’s law?

A

In a mixture of non reacting gases Ptotal = Pa + Pb. (P total is the sum of the pressures of individual gases).

283
Q

What is Boyle’s law?

A

Pressure and Volume are inversely proportional:P1V1 = P2V2.

284
Q

What is Henry’s law?

A

The solubility of a gas is proportional to the partial pressure of the gas. S1/P1 = S2/P2.

285
Q

What is the acid/base dissociation equation?

A

CO2 + H2O = H2CO3 = HCO3- + H+

286
Q

What enzyme catalyses the formation of bicarbonate and hydrogen ions from CO2 and H2O?

A

Carbonic anhydrase.

287
Q

What is the henderson hasselbalch equation?

A

pH = pKa + log (A-)/(HA)

288
Q

What is Laplace’s law?

A

P = 2T/R.

289
Q

What is the significance of Laplace’s law?

A

It tells us that small alveoli have a greater pressure and so air will move from small alveoli to larger alveoli; uneven aeration. (Surfactant can prevent this).

290
Q

Where is surfactant produced?

A

It is produced by type 2 pneumocytes in the alveoli.

291
Q

When is surfactant produced?

A

It starts being produced from 34 weeks gestation and production increases rapidly 2 weeks before birth.

292
Q

List 4 functions of surfactant.

A
  1. Prevents alveoli collapse.2. Allows homogenous aeration.3. Reduces surface tension.4. Maintains functional residual capacity.
293
Q

Premature babies may have surfactant deficiency. What are the consequences of this?

A
  1. Respiratory distress syndrome.2. Non-compliant lungs.3. Unequal aeration.4. Reduced lung volume.
294
Q

How can you treat surfactant deficiency?

A

Ensure the patient is warm and is receiving O2 and fluids. Begin surfactant replacement.

295
Q

Briefly describe the controller-effector-sensor loop.

A

The sensor detects a change (hypoxia), sends signals along the afferent pathway to the controller. The controller then sends signals along the efferent pathway to the effector. The effector responds.

296
Q

What does the pneumotaxic area do and where is it located?

A

It switches off inspiratory neurones and so allows expiration. It is located in the upper pons.

297
Q

What does the apneustic centre do and where is it located?

A

It inhibits expiration by activation inspiratory neurones. It is located in the lower pons.

298
Q

Where are SASR (slow adapting stretch receptors) located?

A

Found in smooth muscle around airways.

299
Q

What activates SASR?

A

Lung distension.

300
Q

How do SASR respond to activation?

A

They inhibit inspiration and so promote expiration.

301
Q

Where are RASR (rapidly adapting stretch receptors) located?

A

Between airway epithelial cells.

302
Q

What activates RASR?

A

Lung distension and irritants.

303
Q

How do RASR respond to activation?

A

Bronchoconstriction.

304
Q

What activates C fibres J receptors?

A

Increased interstitial fluid volume.

305
Q

How do C fibres J receptors respond to activation?

A

They cause rapid, shallowing breathing. Bronchoconstriction and cardiovascular depression.

306
Q

Where are central chemoreceptors located?

A

Medulla oblangata.

307
Q

What stimulates central chemoreceptors?

A

An increase in H+ concentration in the ECF.

308
Q

Where are peripheral chemoreceptors located?

A

Carotid and aortic bodies.

309
Q

What stimulates peripheral chemoreceptors?

A

A decrease in PaO2.

310
Q

What is the respiratory drive more senstitive to, CO2 or O2?

A

It is very sensitive to CO2 and so CO2 is a greater drive. A small change in PaCO2 results in a large ventilatory change.

311
Q

Oxygen dissociation curve: what causes the curve to shift to the right?

A

An increase in temperature and a decrease in pH.

312
Q

Oxygen dissociation curve: what does it mean when the curve shifts to the right?

A

There is increased O2 unloading. Hb’s affinity for oxygen has decreased.

313
Q

Oxygen dissociation curve: what causes the curve to shift to the left?

A

A decrease in temperature and an increase in pH.

314
Q

What is a cause of respiratory acidosis?

A

Inadequate ventilation; could be due to obstruction e.g. COPD.

315
Q

What is the renal compensation mechanism for respiratory acidosis?

A

Increased ammonia formation. H+ secretion increases and there is increased HCO3- reabsorption.

316
Q

What can cause respiratory alkalosis?

A

Hyperventilation in response to hypoxia.

317
Q

What is the renal compensation mechanism for respiratory alkalosis?

A

H+ secretion decreases; more H+ is retained. HCO3- secretion.

318
Q

What is a cause of metabolic acidosis?

A

Renal failure; loss of HCO3-, excess H+ production.

319
Q

What is the respiratory compensation mechanism for metabolic acidosis?

A

Chemoreceptors stimulated, enhancing respiration, PaCO2 decreases.

320
Q

What is the respiratory compensation mechanism for metabolic alkalosis?

A

Chemoreceptors are inhibited, reduced respiration, PaCO2 increases.

321
Q

What is a cause of metabolic alkalosis?

A

Vomiting; loss of H+.

322
Q

Is respiratory compensation fast or slow?

A

FAST!

323
Q

What is type 1 respiratory failure and what are its causes?

A

Hypoxemia. Causes: V/Q mismatch due to alveolar hypoventilation, high altitude, shunt, diffusion problem.

324
Q

What is type 2 respiratory failure and what are its causes?

A

Hypoxemia and hypercapnia. Causes: inadequate alveolar ventilation due to reduced breathing effort, decreased SA, neuromuscular problems.

325
Q

What is forced vital capacity?

A

Volume of air that can be forcibly exhaled after maximum inhalation.

326
Q

How could you diagnose a patient with having an obstructive lung disease?

A

The FEV1/FVC ratio would be less than 70% predicted value.

327
Q

How could you diagnose a patient with having an restrictive lung disease?

A

The FEV1/FVC ratio would be normal but their FVC value would be very low.

328
Q

How can you work out total lung capacity?

A

Add vital capacity to residual volume.

329
Q

What is tidal volume?

A

The volume of air moved into or out of the lungs during normal, quiet breathing.

330
Q

What changes are seen in an aging lung?

A

Decreased compliance, muscle strength, elastic recoil, immune function. Decreased response to hypoxia and hypercapnia. Impaired gaseous exchange.

331
Q

What happens to the FEV1 and FVC in an elderly person?

A

They both decrease and the residual volume increases.

332
Q

What effect does hypoxia have on pulmonary vessels?

A

It vasoconstricts the vessels and so redirects blood to O2 rich alveoli.

333
Q

What is hypersensitivity?

A

Undesirable reaction produced by the immune system.

334
Q

Hypersensitivity: What is the mechanism of a type 1 reaction?

A

Antigens interact with IgE bound to mast cells. Histamine is released. This can cause hayfever, asthma, acute anaphylaxis etc. (Antihistamines are often given as treatment).

335
Q

What is the parasympathetic neurotransmitter in the lungs?

A

Acetylcholine.

336
Q

What is the sympathetic neurotransmitter in the lungs?

A

Noradrenaline.

337
Q

What is the effect of Ach on the pulmonary vessels?

A

Bronchoconstriction and vasodilation.

338
Q

What is the effect of noradrenaline on the pulmonary vessels?

A

Bronchodilation and vasoconstriction.

339
Q

Name 2 receptors for Ach.

A

Muscarinic (G protein coupled) and Nicotinic (ligand gated ion channels).

340
Q

Host defense: What is innate immunity?

A

Immunity that doesn’t require prior exposure. It usually involves phagocytosis and inflammation.

341
Q

Briefly describe the mechanism of inflammation.

A

Vasodilation results in exudation of plasma. Neutrophils and monocytes migrate into tissues.

342
Q

What are alveolar macrophages derived from?

A

Monocytes. They are the resident phagocyte in the lungs and they coordinate inflammatory response.

343
Q

What is the function of the epithelial barrier in host defense?

A

Moistens and protects airways. Functions as a barrier to pathogens and foreign matter.

344
Q

What is the muco-ciliary escalator?

A

Mucosal secretions from goblet cells and submucosal glands trap particulate matter. The beating cilia transport the mucus up the respiratory tract. This acts to prevent infection.

345
Q

What is coughing?

A

An explosive expiration that acts to clear foreign matter from the airways. It is an important defense mechanism.

346
Q

What does the lung bud form from?

A

The respiratory diverticulum - an out-pouching of the fore gut.

347
Q

What is the septum called that seperates the lung bud from the oesophagus in the embryo?

A

Tracheoesophageal septum.

348
Q

What are the 5 stages of respiratory tract development called? What happens in these stages?

A
  1. Embryonic (0-5 weeks): lungs and trachea develop.
  2. Pseudoglandular (5-16 weeks): branching of trachea.
  3. Canalicular (16-26 weeks): Respiratory bronchioles form.
  4. Saccular (26w-birth): Terminal sacs form.
  5. Alveolar (8 months to childhood): Alveoli mature.
349
Q

Describe the first breath.

A
  1. Fluid is removed from the lungs.2. Adrenaline increases surfactant release.3. Air is inhaled. 4. O2 VASODILATES pulmonary vessels. 5. Umbilical arteries and ductus arteriosus constricts. Foramen ovale closes.
350
Q

Define anatomical dead space.

A

The volume of air taken in during a breath that does not enter the alveoli.

351
Q

Define physiological dead space.

A

The volume of air that is taken in during a breath that does not take part in gas exchange.

352
Q

What it total lung capacity equal to?

A

TLC = VC + RV.

353
Q

Where is the basic neural machinery for the generation of the respiratory rhythm located?

A

In the lower medulla.

354
Q

True or False: the intercostals are the main muscles of respiration.

A

False - the diaphragm is the main muscle of respiration.

355
Q

Which alveoli are preferentially ventilated and perfused?

A

Those at the base of the lungs.

356
Q

Why can hypoxia cause respiratory alkalosis?

A

Hypoxia leads to hyperventilation as the person tries to inhale more O2. This means you lose a lot of CO2 resulting in alkalosis.

357
Q

Define total lung capacity.

A

The vital capacity plus the residual volume. It is the maximum amount the lungs can hold.

358
Q

Define residual volume (RV).

A

The volume of air remaining in the lungs after a maximal exhalation.

359
Q

Define functional residual capacity (FRC).

A

The volume of air remaining in the lungs after a tidal volume exhalation.

360
Q

Define tidal volume (TV).

A

The volume of air moved in and out of the lungs during a normal breath.

361
Q

Define FEV1.

A

The volume of air that can be forcibly exhaled in 1 second.

362
Q

What 2 equations can be used to work out TLC?

A
  1. TLC = VC + RV.2. TLC = TV + FRC + IRV.
363
Q

Define forced vital capacity (FVC).

A

The maximum volume of air that can be forcibly exhaled after maximal inhalation. Usually in 6 seconds.

364
Q

Define expiratory reserve volume (ERV).

A

The additional volume of air that can be forcibly exhaled after a tidal volume expiration.

365
Q

Define inspiratory reserve volume (IRV).

A

The additional volume of air that can be forcibly inhaled after a tidal volume inspiration.

366
Q

What is lung compliance?

A

A measure of the lung’s ability to stretch and expand. Compliance = ∆V/∆P.

367
Q

Why do you see decreased elastic recoil in an ageing lung?

A

The elastin degenerates and ruptures.

368
Q

Why do you see decreased muscle strength in an ageing lung?

A

There is a decrease in type 1, fatigue resistant fibres. And muscle mass also decreases.

369
Q

Why do you see a decreased response to hypoxia and hypercapnia in an ageing lung?

A

The lung is more vulnerable and has a decreased awareness meaning these changes aren’t detected till late on.

370
Q

Why do you see decreased immune function in an ageing lung?

A

There is less protective mucus and sputum clearance is less effective.

371
Q

Why do you see impaired gaseous exchange in an ageing lung?

A

The SA for gaseous exchange decreases and there is increased V/Q mismatch.

372
Q

Why does the residual volume increase in an ageing lung?

A

The chest wall changes shape. There is increased calcification and stiffness.

373
Q

What is the main cell involved in acute inflammation?

A

Neutrophils.

374
Q

What can the pneumotaxic area override?

A

The apneustic area.

375
Q

Name 4 non-immune host defense mechanisms.

A
  1. Mucus.2. Muco-cilliary escalator.3. Epithelium.4. Cough.
376
Q

What layer of the tri-laminar disc is the respiratory tract derived from?

A

The endoderm.

377
Q

What is the respiratory diverticulum an out-pouching of?

A

The foregut.

378
Q

What does the respiratory diverticulum go on to form?

A

The lung buds.

379
Q

Give 2 ways that oxygen is carried around the body?

A
  1. Bound to Hb.2. Dissolved in blood.
380
Q

What is Hb affinity for O2?

A

How readily Hb acquires and releases O2 at respiring tissues.

381
Q

Does the umbilical vein carry oxygenated blood or deoxygenated?

A

Oxygenated (umbilical artery carries deoxygenated).

382
Q

What is the importance of the ductus venosus in foetal circulation?

A

It is used to bypass the liver. Oxygenated blood from the umbilical vein can go straight to the IVC and not through the liver.

383
Q

Define vital capacity.

A

The maximum volume of air that can be exhaled after a maximal inhalation.

384
Q

What is the normal tidal volume in an adult?

A

500ml.

385
Q

What cell type lines most of the surface of an alveoli?

A

Type 1 pneumocytes. Type 2 are more numerous but type 1 are squamous and so are responsible for more of the SA.

386
Q

What is the thickness of the air-blood barrier in nm?

A

200-800 nm.

387
Q

What is the epithelium of the vocal cords?

A

Stratified squamous non-keratinising.

388
Q

What is the base, apex and roof of the maxillary sinus formed from?

A

Base - lateral wall of the nose. Apex - zygomatic process of the maxilla. Roof - floor of the orbit.

389
Q

Which sinus is a labyrinth of air cells?

A

The ethmoid.

390
Q

What vertebral level does the larynx extend to?

A

C6.

391
Q

True or False: alveolar macrophages release interleukins.

A

True - this is important in the coordination of an immune response.

392
Q

Why does constriction of bronchioles cause significant increase in airway resistance and can cause an expiratory wheeze such as seen in asthma?

A

Bronchioles have no cartilage, only smooth muscle. This means they are more likely to constrict and increase airway resistance.

393
Q

Which respiratory tract structures are lined with smooth muscle and contain no cartilage?

A

Bronchioles.

394
Q

Define peak expiratory flow (PEF).

A

The greatest rate of airflow that can be obtained during forced exhalation.

395
Q

Define airway obstruction.

A

Impediment to inspiratory and expiratory air flow.

396
Q

Define airway restriction.

A

When the lungs are restricted from full expansion.

397
Q

Anaphylaxis is caused by the cross-linking of an immunoglobulin on the surface of an inflammatory cell, resulting in the release of a potent chemical mediator. State the class of the immunoglobulin, the name of the cell and the name of the chemical mediator.

A

IgE

Mast Cell

Histamine

398
Q

What are broncho-pulmonary segments?

A

Discrete functional and anatomical units of the lung. Each segment is supplied by a specific segmental/tertiary bronchus.

399
Q

How many broncho-pulmonary segments are there in the right lung?

A

10

400
Q

How many broncho-pulmonary segments are there in the left lung?

A

8

401
Q

What effect does hypoxia have on systemic vessels?

A

Vasodilation.

402
Q

How do we recognise pathogens we have nerve seen before?

A

Pattern recognition receptors - PRRs.

403
Q

What are the causative agents of acute inflammation?

A

Pathogens, damaged tissue.

404
Q

What are the causative agents of chronic inflammation?

A

Persistent acute inflammation, persistent foreign bodies, autoimmune reactions.

405
Q

What are main cells involved in acute inflammation?

A

Neutrophils! Also eosinophils and basophils.

406
Q

What are main cells involved in chronic inflammation?

A

Mononuclear cells e.g. monocytes, macrophages, lymphocytes, plasma cells.

407
Q

What are the primary mediators in acute inflammation?

A

Vasoactive amines.

408
Q

What are the primary mediators in chronic inflammation?

A

Cytokines, growth factors, ROS etc.

409
Q

What are the outcomes of chronic inflammation?

A

Tissue destruction, fibrosis, necrosis, chronic inflammation.

410
Q

What are the outcomes of acute inflammation?

A

Resolution.

411
Q

What suppresses alveolar macrophage activation in a healthy lung?

A

Respiratory epithelium.

412
Q

Which results in inflammation, necrosis or apoptosis?

A

Necrosis.

413
Q

Why is the lung at increased risk of inflammation?

A
  1. Huge area in contact with the external environment.2. The lung contains the majority of our WBC’s at any one time.
414
Q

What is the function of mucus?

A

It protects the epithelium from foreign material and from fluid loss.

415
Q

What mechanism moves airway mucus up into the throat?

A

Muco-ciliary escalator.

416
Q

What is mucus composed of?

A

Water, carbohydrates, lipids and proteins.

417
Q

Name 4 non-immune host defence mechanisms.

A
  1. Epithelial barrier. 2. Mucus. 3. Muco-ciliary escalator. 4. Coughing.
418
Q

What nerves does the efferent limb of the cough reflex include?

A

Recurrent laryngeal and spinal nerves.

419
Q

What nerves does the afferent limb of the cough reflex include?

A

Receptors within the sensory distributions of Cn 5, 9 and 10.

420
Q

What is adaptive immunity?

A

An antigen-specific immune response.

421
Q

What is the function of B cells?

A

Antibody production.

422
Q

Name 3 types of T cells.

A
  1. Cytotoxic T cells. 2. Helper T cells. 3. Memory T cells.
423
Q

What is the function of cytotoxic T cells?

A

They track down infected cells.

424
Q

What is the function of helper T cells?

A

they secrete cytokines to attract macrophages and neutrophils etc.

425
Q

What can cause a type 1 hypersensitivity reaction?

A

Pollen, cat hair, peanuts (allergies).

426
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection, transfusion mismatch.

427
Q

What can cause a type 3 hypersensitivity reaction?

A

Fungal.

428
Q

What can cause a type 4 hypersensitivity reaction?

A

TB.

429
Q

What are the functions of lymphocytes?

A

They make antibodies, decide what type of antibodies to make and kill diseased cells.

430
Q

What is the Gell and Coombs classification?

A

It describes 4 types of hypersensitivity reaction.

431
Q

Describe the mechanism and give examples of a type 1 hypersensitivity reaction.

A
  • Mechanism: immunological memory to something causing an allergic response. IgE antibodies bind to mast cells -> histamine release. - Anaphylaxis, hayfever etc. Can be caused by pollen, allergens.
432
Q

Describe the mechanism and give examples of a type 2 hypersensitivity reaction.

A

NAME?

433
Q

Describe the mechanism and give examples of a type 3 hypersensitivity reaction.

A
  • Mechanism: immune complexes, activation of complement. - Fungi and pigeon droppings etc. (pigeon fancier’s lung).
434
Q

Describe the mechanism and give examples of a type 4 hypersensitivity reaction.

A

NAME?

435
Q

What comprises a respiratory acinus?

A

Respiratory bronchiole, alveolar duct and alveolus.

436
Q

What part of the respiratory tract lies behind the sternal angle?

A

The tracheal bifurcation.

437
Q

Give an example of a restrictive lung disease?

A

Pulmonary fibrosis.

438
Q

Give an example of an obstructive lung disease?

A

Chronic bronchitis and emphysema.

439
Q

What is the affect of pulmonary fibrosis on the following: FEV1, FVC, PEF, TLC and DLCO?

A

All reduced except PEF which is non variable

440
Q

What is the affect of emphysema on the following: FEV1, FVC, PEF, TLC and DLCO?

A
  • FEV1 = reduced. - FVC = normal or slightly reduced. - PEF = typically not variable. - TLC = increased (hyperinflation). - DLCO = reduced.
441
Q

What is the affect of asthma on the following: FEV1, FVC, PEF, TLC and DLCO?

A

NAME?

442
Q

What is DLCO?

A

Uptake of CO in ml at standard temperature and pressure.

443
Q

Define inspiratory capacity (IC).

A

The maximum volume of air that can be forcibly inspired - IC = TV + IRV.

444
Q

What are the 6 stages of neutrophil action?

A
  1. Identify threat.2. Activation. 3. Adhesion. 4. Migration. 5. Phagocytosis. 6. Bacterial killing.
445
Q

What is the consequence of mucus plugs in the lungs?

A

Airway obstruction which can ultimately lead to death.

446
Q

What is the equation for trans-pulmonary pressure?

A

Transpulmonary pressure = alveolar pressure - pleural pressure. (TPP is always positive).

447
Q

What layer of the trilaminar disc is pleura derived from?

A

Mesoderm.

Year 1 Medicine (25 decks)

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