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Medicine Phase 1 mine > 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

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4
Q

Describe the Turbinates and area around them.

A

Superior meatus - olfactory epithelium, cribriform plate and sphenoid sinus.
Middle has semi-lunaris sinus openins and inferior as nasolactimal duuct

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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 hiatus semilunaris

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8
Q

Ethmoid sinus describe it.

A

they are labyrinthine between the eys through the semilunar hiatus as well opthalmic and maxillary trigeminal nerve

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9
Q

Sphenoid sinus

A

is medial to the cavernous sinus inferior to optic canal duran and pituitary gland it empties into the sphenoethmoidal recess lateral to the nasal septum innervated by opthalmic divison 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 suplies all of the innervation to the larynx.
there are two branches the Superior laryngeal nerve and the recurrent larengeal nerve.
The superior larengeal provides sensory to above the glottis and the external branch does the motor inntervation to cricothyroid.
the recuurant larengeal nerve provides sensort 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 lower(with linguilla)

Left upper, middle and lower lobe

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20
Q

What are the divisions of the lungs?

A

lungs lobes segments

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21
Q

name the airways names

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) receptorsparietal is on walls has pain sensation

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25
Q

What is the bronchial circulation?

A

Bronchial circulation, is the blood suply to yhe lung and the pulmonary arteries follow the bronchi.

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26
Q

What is the rough svolume 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

Vdot A V dot CO2 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 equation for arteriolar CO2

A

k times Vdot CO2 (prod)/ Alveolar ventilation

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39
Q

What is the alveolar gas equation?

A

PAO2=PiO2- PaCO2/Resp quotient.

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40
Q

What cause hypoxaemia low O2

A

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

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41
Q

What factors affect binding of Oxygen with Haemoglobin?

A

CO, 2,3 DPG, pH, temperature

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42
Q

What does carbonic anhydrase catalyse?

A

The joining of carbon dioxide and water.

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43
Q

What are the non immune defences of the lung?

A

Cough nasal hairs mucus cilia

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44
Q

What are the features of inflamation?

A

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

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45
Q

What are the physcial 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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46
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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47
Q

What is the cause of COPD?

A

smoking fossil fuels etc but due to inflamation in the lungs

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48
Q

What is ARDS?

A

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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49
Q

Adaptive immune cells are made where?

A

in the bone marrow

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50
Q

What is the origin of the blood cells?

A

haematopoeitic stem cells.

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51
Q

How does inflamation become initiated?

A

The epithelium produces hydrogen peroxide when dammaged. this response is amplified by specialist macrophages like Kupffer alveolar macrophages histocytes. the response is done by recognising pathogen associated molecular patterns or damage associated molecular patterns.

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52
Q

What are alveolar macrophages?

A

They are macrophages that absorb bacteria and probe environment there are many difference with macrophages within one tissue.

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53
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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54
Q

How can neutrophils be turned off?

A

macrophages can absorb neutrophils and change type.

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55
Q

what are the roles of neutrophils?

A

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

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56
Q

Describe the neutrophil receptors?

A

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

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57
Q

Describe nutrophil activation

A

stimulus response coupling, signal transduction pathways and release granules

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58
Q

Describe neutrophil adhesion

A

margination- selectins where they go to endothelium, adhesion integrins to migrate through the wall require a change in neutrophil and endothelium

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59
Q

Describe neutrophil migration

A

ability to dectect concentration gradient and move along the gradient

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60
Q

Describe phagocytosis

A

invagination called phagoome, and granules joing called a phagolysosome

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61
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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62
Q

What is airway tone?

A

the contraction or relaxation of muscle in the airways.

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63
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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64
Q

What regulates the airways smooth muscle tone?

A

the autonomic nervous system and is regulated by inflamation.

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65
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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66
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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67
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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68
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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69
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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70
Q

What is a SABA?

A

Short acting beta2 agonists such as salbutamol.

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71
Q

What is a LABA?

A

Long acting beta 2 agonist like salmeterol or formoterol.

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72
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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73
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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74
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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75
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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76
Q

What are the goals of asthma treatment?

A

Get control of symptoms, relief of symptoms

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77
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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78
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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79
Q

What are the three levels of defence in the lung?

A

intrinsic, innate, and adaptive

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80
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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81
Q

What is the biggest defence in the lungs?

A

mucus production and release with cilliary escalator

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82
Q

What is the host defence in the alveolar gas exchange?

A

surfactant and a physical barrier

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83
Q

What is periculliary fluid?

A

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

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84
Q

What is coughing?

A

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

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85
Q

What is sneezing?

A

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

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86
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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87
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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88
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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89
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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90
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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91
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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92
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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93
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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94
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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95
Q

How can total lung volume be measured?

A

Gas dilution- doesnt measure air in communicating bullae closed circuit helium or open circuit nitrogen washout. with helium known amount added and when you breath out measures concentration
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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96
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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97
Q

What is a low FEV1?

A

Anything about 80% or greater of you predicted value.

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98
Q

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

A

Airways restriction.

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99
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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100
Q

What does an astmatic flow volume loop?

A

the lower one is scalloped and the FEV1 is lower

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101
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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102
Q

What are the flow loop for a COPD patient?

A

scalloped and lower PEF.

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103
Q

What are the symptoms 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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104
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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105
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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106
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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107
Q

What are clinical symptoms of pulmonary fibrosis?

A

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

108
Q

Blood gasses for pulmonary fibrosis?

A

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

109
Q

What causes the urge to breath?

A

Carbon dioxide sensors in health

110
Q

What is a normal respiratory rate?

A

10-12 breaths per minute

111
Q

What proportion of blood goes through the bronchial circulation?

A

2%

112
Q

What is the surface area of gas exchange roughly?

A

50-100m^2

113
Q

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

A

Thin walls in pulmonary thich in systemic highly muscularise systemic less so in pulmonary, lots of redistribution in systemic and pulmonary not as much.

114
Q

What is Pousieuille’s Law?

A

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

115
Q

What is Ohm’s law?

A

Pressure in circuit= Cardiac output x resistance

Pressure across pulmonary circulation = mPAP-left arterial pressure pulmonary vascular resistance

116
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.

117
Q

What is hypoxaemia?

A

The lack of sufficient blood in the blood

118
Q

What are the two types of respiratory failure defined as?

A

Type 1 pO2 is below 8kPA pCO2 is less than 6kPA

Type 2 pO2 is below 8kPA pCO2 is above 6kPA

119
Q

What are the main causes of hypoxaemia?

A

Hypoventilation, Diffusion impairment, Shunting, V/Q mismatch

120
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.

121
Q

What is diffusion impairment?

A

When the gases struggle to pass across the membrane.. Pulmonary oedema can resuce gaseous diffusion, blood diffusion is anaemia, membrane diffusion is interstitial fibrosis.

122
Q

What is V/Q mismatch?

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

123
Q

What is a shunt?

A

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

124
Q

What are causes of shunts?

A

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

125
Q

What is hypoxic pulmonary vasoconstriction?

A

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

126
Q

what are diseases of pulmonary circulation.

A

Pulmonary embolism, pulmonary hypertention pulmonary AVM

127
Q

Where does the lung develop from?

A

the foregut ventral outpouching in the 5th week

128
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

129
Q

What happens after 17 weeks to 25 weeks of lung development?

A

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

130
Q

What happens upto birth?

A

get alveolar sacs develop two types for cells.

131
Q

when does lung development stop?

A

At about 5 years old

132
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

133
Q

What can go wrong in canalicular stage?

A

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

134
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

135
Q

What is oxygen in the pulmonary circulation?

A

it is a vasoconstrictor.in lungs blood chases oxygen.

136
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

137
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

138
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.

139
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

140
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.

141
Q

What is Laplace’s law?

A

Pressure= 2T/radius more pressure to inflate a small sphere. surface tension tries to colapse the lungs the surfactant changes this.

142
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.

143
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.

144
Q

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

A

Gel and coumbs

145
Q

What are cytokines?

A

Proteins that allow leukocytes and tissue cells to talk to eachother

146
Q

Where do antigen presenting cells go?

A

to the lymph nodes

147
Q

When are IgM antibodies made?

A

at the beginning of an infection

148
Q

What are IgG?

A

highly specific that targed specific epitopes

149
Q

What are Ig E?

A

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

150
Q

Where can IgA be found?

A

It can be found in mucous membranes

151
Q

Outline the Gell and coombs calcifications

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

152
Q

Describe Type 1 reactions immune

A

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

153
Q

What is Atopy?

A

inherited tendency to exaggerated IgE response to an antigen. 25% havegenes but less than half of these

154
Q

What is anaphalaxis usually linked with?

A

IgE and histamine attaching to mast cells

155
Q

How is atopy diagnosed?

A

Skin prick tests, RAST radio

156
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.

157
Q

What is a type three hypersensivity?

A

Formation of precipitating antobodies to organic dust which form granulomas in the lung.

158
Q

What is a type 4 reaction?

A

formation of granulmas and depends on activation of T Cells.

159
Q

What are some common causes of hypersensitivity

A

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

160
Q

What are some common lung diseases that are genetically linked?

A

Cystic fibrosis, Alpha-1 antitrypsin deficiency

161
Q

How do genetics and disease presentation link?

A

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

162
Q

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

A

around 19/20 steepest growth is after 10 years

163
Q

At what age is it expected that lung function peaks?

A

At around 20-25 years old

164
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.

165
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.

166
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

167
Q

What does the treatment of CF include?

A

Rescue when exacerbations occur, prevention or maintenance treatment

168
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

169
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

170
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.

171
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

172
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.

173
Q

Why is PaCO2 more important?

A

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

174
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.

175
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.

176
Q

What do the Pneumotaxic and apneustic centre do?

A

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

177
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.

178
Q

What is the central pattern generator?

A

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

179
Q

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

A

central 60%, peripheral40%.

180
Q

What is the primary influence in central chemo receptors?

A

PaCO2

in carotids it is PaCO2 and PaO2 and pH.

181
Q

Where are the central chemoreceptors?

A

in the pontomedullary junction.

182
Q

Why are central chemoreceptors more sensitive to PaCO2 than H+

A

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

183
Q

In the brain how are CO2 levels sensed?

A

By the H+ concentration from carbonic anhydrase,

184
Q

Where are the carodid and aordic bodies?

A

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

185
Q

Whats the main sensor of oxygen?

A

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

186
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.

187
Q

What are irritant receptors like?

A

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

188
Q

What are J receptors?

A

Juxtapulmonary capillary the have C fibres

189
Q

Where are some other receptors?

A

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

190
Q

what are the muscle proprioceptors?

A

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

191
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.

192
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
193
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.

194
Q

What is intersting about oxygen pressure changes?

A

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

195
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.

196
Q

What are the three common altitude problems?

A

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

197
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.

198
Q

What is high altitude pulmonary oedema?

A

Unacclimatised individuals cough shortness of breath, from rapid ascent abover 2500m, 2-5 days risk lowered by slowing ascent sleeping lower exercising and respiratory tract infection. increases
To treat recompress oxygen steroids calcium blockers?

199
Q

What is high altitude cerebreal oedema?

A

Serious Confusion behaviour change, Immediate descent, symptoms can resolve relatively quickly.

200
Q

What can be done for people flying?

A

give oxygen

201
Q

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

A

10m= 1ATM

202
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.

203
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.

204
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

205
Q

What is the diving reflex?

A

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

206
Q

What does SCUBA stand for?

A

Self-contained underwater breathing apparatus.

207
Q

What has to be considered with the gas canisters?

A

what ambient pressure you will be breathing the gas at.

208
Q

What is Dalton’s Law?

A

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

209
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.

210
Q

How can you assess CNS oxygen toxisity?

A 
VENTID
Vision
Ears(tinitus)
Nausea
Twitching
Irritaility
Dizzines
convulsions
211
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.

212
Q

What is decompression illness?

A

N2 is usually poorly soluble but as you elevate again the bubbles increase and cause problems it can cause rashes (cutaneous marmaladosis) type one cutaneous type 2 neurological

213
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

214
Q

What is pulmonary barotrauma?

A

Air leaks from burst alveoli into thorax(pneumothorax) medistinum (pneumomediastinum or get subcutaneous emphysema.

215
Q

What can cause lung problems?

A

Allergens Infection.

216
Q

What is asthma?

A

Chronic inflamatory disease inflamationin the airways.

217
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.

218
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.

219
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.

220
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

221
Q

What is the initial innate immune response to pathogens?

A

lt reacts quickly but in the same way each time

222
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

223
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.

224
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.

225
Q

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

A

T cells- secret cytokines, cytotoxicity and regulate

B cells- release antibodies(immunoglobulins)

226
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

227
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.

228
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.

229
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.

230
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.

231
Q

Why is tolerance to self needed?

A

To stop auto immune responses being devloped and in pregnancy.

232
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.

233
Q

What is peripheral tolerance?

A

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

234
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

235
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)

236
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.

237
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.

238
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.

239
Q

What is an IgM ?

A

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

240
Q

What do IgA do?

A

dimer that can accesss mucosal surfaces and mediates mucosal immunity

241
Q

What to IgG and IgE do?

A

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

242
Q

What are some of the effects of antibodies?

A

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

243
Q

How is the immune response harnessed in vaccinations?

A

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

244
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

245
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

246
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.

247
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.

248
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

249
Q

What is vasulitis?

A

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

250
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

251
Q

What are the three patterns of chronic inflamation?

A

Suppurative inflamation where the cells are surrounded by a capsule of inflamatory cells or fibrous tissue
autoimmune inflamation can lead to fibrosis
granulomatous cells can leat to fibrosis as well.

252
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

253
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

254
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

255
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.

256
Q

What is the treatment for chronic inflamation.

A

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

257
Q

What does the parasympathetic nervous system do to the lungs?

A

Constricts bronchi

258
Q

What does the sympathetic nervous system do to the lungs?

A

It dilates the bronchi

259
Q

What causes bronchoconstriction?

A

Parasympathetic nervous sytem

260
Q

What neurotransmitters are involved with bronchoconstriction/

A

Acetyl choline at both synapses

261
Q

What receptor causes bronchoconstriction?

A

ACh acting on M3 muscarinic receptors

262
Q

What are the treatments for bronchoconstriction?

A

Anticholinergic, muscarinic antagonists

263
Q

What receptor mediates smooth muscle relaxation?

A

Beta 2 adrenergic receptors

264
Q

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

A

Noradrenaline

265
Q

What are the types of adrenergic receptors?

A

Alpha and Beta,

Medicine Phase 1 mine (21 decks)

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