Respiratory Flashcards
1
Q
What is the most superior portion of the respiratory tract?
A
The nose/nasal cavity
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.
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
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
5
Q
What are the names of the sinuses?
A
Frontal, Maxillary, ethmoid and sphenoid
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
7
Q
Describe the mailiary sinus
A
opens into the middle meatus through the semilunar hiatus
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
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
10
Q
what are the boundaries and sections of the pharynx
A
skull base to C6, split into nasopharynx oropharynx and laringopharynx
11
Q
What happens in the nasopharynx
A
Eustachian tube enders with the ears
12
Q
What are the names of the laryngeal cartilages?
A
Single- epiglottis, theyroid and cricoid
Double- Cuneiform Corniculate and Arytenoid
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
14
Q
Where is the Carina?
A
T4/5
15
Q
What shape is the trachea?
A
Oval
16
Q
What shape are tracheal cartilages?
A
Semicircular cartilages
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
18
Q
What is the lingular lobe?
A
probably reminant of left middle lobe
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)
20
Q
What are the divisions of the lungs?
A
lungs lobes segments
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.
22
Q
What is the lung acinus?
A
Functional unit of the lung made of many small alveoli
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
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
25
What is the bronchial circulation?
Bronchial circulation is the blood supply to the lung tissue and the pulmonary arteries follow the bronchi.
26
What is the rough volume of air through the lungs in a minute?
5litres
27
which nerve innervates the diaphragm?
the phrenic C3,4,5
28
What is the significance of the interpleural space?
has a few mililitres of fluidto lubricate its is a potential space
29
What is ventilation and perfusion?
ventilation is the movement of air in and out of the lung. perfusion is a blood supply to the area of the lung.
30
What is dead space?
volume of air not contributing to ventilation?
31
What are the divisions of dead space?
Anatomic 150mls and alveolar 25mls isn't much blood there so physiological dead space is both 175ml
32
What can affect the perfusion of a lung?
pulmonary artery pressure, pulmonary venous pressure and alveolar pressure.
33
What is hypoxic pulmonary vasoconstriction?
when there are low levels of oxygen in the lung the vessels constrict
34
PaCO2, PACO2 Pi O2 mean what?
arterial CO2 alveolar CO2 pressure of inspired O2
35
VA VCO2 mean what?
alveolar ventilation and CO2 production
36
How is CO2 carried in the blood?
Dissolved in plasma, Attached to haemoglobin and as carbonic acid
37
What are physiological causes of high CO2?
reduced minute ventilation, shallow rapid breathing as lots is dead space, Vdot A reduced by increased dead space ventilation, Increased CO2 production
38
What is the alveolar gas equation?
PAO2=PiO2- PaCO2/Resp quotient.
39
What cause hypoxaemia low O2
Alveolar hypoventilation, reduced O2 pressure V/Q mismatch and diffusion abnormality.
40
What factors affect binding of Oxygen with Haemoglobin?
CO, 2,3 DPG, pH, temperature
41
What does carbonic anhydrase catalyse?
The joining of carbon dioxide and water.
42
What are the non immune defences of the lung?
Epithelium
Nasal Hairs
Mucous
Mucociliary escalator
Cough
43
What are the clinical features of inflamation?
Calor (heat) Rubor (redness) Dolor (pain) Tumour (swelling) Functio laesa (loss of function)
44
What are the physiological inflamatory features?
Vasodilatation leadint to more plasma exudation, activation of biochemical cascades, migration of leukocytes into the tissues such as neutropils and monocytes
45
What is the double edged sword in body's response to disease?
Inflamation fights infection but lots of people will die from inflamation.
46
What is the cause of COPD?
smoking fossil fuels etc but due to inflamation in the lungs
47
What is ARDS?
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
48
Adaptive immune cells are made where?
in the bone marrow
49
What is the original cell of the blood cells?
haematopoeitic stem cells.
50
What percentage of wbc are neutrophils?
70%80 millin are made each minute. they contain granules wich release myeloperoxidates elastase or secondary receptors lysoszyme and collagenase
51
How can neutrophils be turned off?
macrophages can absorb neutrophils
52
what are the roles of neutrophils?
activation after identification, adhesion, migration/chemotaxis, phagocytosis, bacterial killing
53
What do neutrophil receptors recognise?
PAMPs and DAMPs
recognise cell walls lipids and peptides of bacteriahost mediator cytokines host opsonins like immunoglobulins. and adhesion molecules
54
Describe neutrophil activation
stimulus response coupling, signal transduction pathways and release granules
55
Describe neutrophil adhesion
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.
56
Describe neutrophil migration
ability to dectect concentration gradient and move along the gradient
57
Describe phagocytosis
invagination called phagoome, and granules joing called a phagolysosome
58
Describe neutrophil bacteral killing
lysosomal enzymes elastase and reactive oxygen species. ROS generated there are many and genetic prolems can affect.
59
What is airway tone?
the contraction or relaxation of muscle in the airways.
60
What are some differences between asthma and COPD?
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
61
What regulates the airways smooth muscle tone?
the autonomic nervous system and is regulated by inflamation.
62
Describe the effect of the parasympathetic nervous system on the airways
it causes bromchoconstriction the vagus nerve does this, they release acetyl choline which acts on muscarinic receptors(M3) in muscle cells.
63
How can excessive bronchoconstriction be treated?
You use drugs that inhibit/ block the M3 receptor called anti-cholinergics or anti-muscarinics
64
What are SAMAs?
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
65
What is a LAMA?
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
66
What is the effect of the sympathetic nervous system on the airways?
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
67
What is a SABA?
Short acting beta2 agonists such as salbutamol.
68
What is a LABA?
Long acting beta 2 agonist like salmeterol or formoterol.
69
How are SABA/LABAs given for asthma?
With steroids, uses in acute rescue of bronchoconstriction and to prevent bronchoconstriction which reduces rates of exacerbations
70
What are the adverse effects of Beta2 agonists?
drives potassium into the cells so causes low levels in the blood, it can increase the heart rate. can cause hyperglycaemia.
71
What is the main factor the governs drug deposition and other factors?
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
72
What is important about asthma treatment?
concordance is low, inhaler education is key and correct device selection is vital
73
What are the goals of asthma treatment?
Get control of symptoms, relief of symptoms
74
What are the immeiate management of asthma?
Oxygen up to 60%, Salbutamol nebuliser prednisolone(steroid tablet), give magnesium or aminiphylline IV
75
What are the functions of the lungs?
Oxygenation of blood, release of carbon dioxide, synthesis activation and inactivation of vasoactive substances, hormones, neuropeptides, lung defence speech vomiting defecation childbirth
76
What are the three levels of defence in the lung?
intrinsic, innate, and adaptive
77
What are some of the nonspecfic defence mechanisms in the respiratory system.
Anti-proteases lysoszomes phospholipase A, Anti fugal peptides ant microbial peptides, surfactant that can opsonize pathogens for phagocytosis. there are also non-pathogenic bacteria.
78
What is the biggest defence in the lungs?
mucus production and release with cilliary escalator
79
What is the host defence in the alveolar gas exchange?
surfactant and a physical barrier
80
What is pericilliary fluid?
the fluid around the cilia wafts the fluid and the mucous moves over the top.
81
What is coughing?
reflext to expell foreign bodies, or an irritating particulate. can be volunatry and involuntary
82
What is sneezing?
it is an involuntary expulsion of nasal irritation. from pollen smoke or too much fluid.
83
How do cells come back after dammage?
spreading and dedifferentiation and then cell migration and proliferation and re differentiation but doesn't get fully better. this is functional plasticity
84
what happens if a bronchiole is blocked?
the gas exchange is blocked, then bacteria and bad can't get out causes infection.
85
What can cause a mucus plug?
goblet cell metaplasia where there are too many goblet cells due to tissue damage.
86
What are the named volumes on a analysis graph that you might have?
Total lung capacity, vital capacity, residual volume, inspiratory reserve volume, expiratory reserve volume, forced tidal volume, functional residual capacity, inspiratory capacity.
87
What are other measured values?
FEV1 forced expiratory volume in one second, FVC forced vital capacity, peak expiratory flow, lung volumes transfer factor estimates
88
What is the difference between volume time and flow volume plots?
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.
89
What are important things to note on flow/volume plot?
Peak flow is top point, FEF is the flow at when 25% has been exhaled.
90
What are the units for peak flow?
L/min. can use a peak flow or spirometer. they need to blow very hard! (effort dependent)
91
What are the problems with measuring the total lung capacity?
can't expel all the air in the lungs only the forced vital capacity.
92
What methods can be used to measure total lung volume?
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.
93
How can we estimate transfer rates?
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.
94
What is a low FEV1?
Anything about 80% or greater of you predicted value.
95
What is it called when FVC is lower than 80% of predicted value?
Airways restriction.
96
What is FEV1/FVC when its lower called?
less than 0.7 is airways obstruction this reduces with age.
97
What does an asthmatic flow volume loop look like?
the lower one is scalloped and the FEV1 is lower
98
What are the blood gases in acute asthma?
PaO2 normal, Pa CO2 low,pH normal or elevated,HCO3 normal
99
What are the flow loop for a COPD patient?
scalloped and lower PEF.
100
What are the test results of asthma?
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
101
What are the symptoms of COPD?
FEV1 reduced significantly, FVC may be normal or reduced, PEF not variable, MEF low scalloped shape, Low transfer rates.
102
What is dynamic hyperinflation?
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
103
What is COPD blood gas like?
low PaO2 High Pa CO2 in type 2 low in type 1 pH normal may have elevated HCO3 if chronic acidosis is present.
104
What are test results of pulmonary fibrosis?
Reduced significanly reduced FEV1 FVC. stable PEF low or normal MEF, TLC reduced low transfer measures normal eNO.
105
Blood gasses for pulmonary fibrosis?
PaO2 is low, Pa CO2 low, pH normal, HCO3 low.
106
What causes the urge to breath?
Carbon dioxide sensors in health
107
What is a normal respiratory rate?
12-20 breaths per minute
108
What proportion of blood goes through the bronchial circulation?
2%
109
What is the surface area of gas exchange roughly?
50-100m^2
110
What are the differences between the systemic system and pulmonary vasculature in the lungs?
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.
111
What is Pousieuille's Law?
Resistance = 8xLxviscocity/Pi r^4 so the bigger the radius of the vessel the less the resistance.
112
What happens to to reduce resistance in the lungs?
Recruitment with more blood vessels and the vessels can distend this can maintain pressure when then cardiac output is increased.
113
What is hypoxaemia?
The lack of sufficient oxygen in the blood
114
What are the two types of respiratory failure defined as?
Type 1 pO2 is below 8kPA pCO2 is less than 6kPAType 2 pO2 is below 8kPA pCO2 is above 6kPA
115
What are the main causes of hypoxaemia?
Hypoventilation, Diffusion impairment, Shunting, V/Q mismatch
116
What is usually the cause of type 2 respiratory failure?
Hypoventilation which can be due to muscular weakness, Obesity, Loss of respiratory drive.
117
What is diffusion impairment?
When the gases struggle to pass across the membrane.. Pulmonary oedema, anaemia, interstitial fibrosis
118
What is V/Q mismatch in a normal Physiological lung?
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
119
What is a shunt?
when there is a blockage to an airway or artery causing a v/Q mismatch.
120
What are causes of shunts?
Bronchial artery blockage Ventricular septal defect, Arterio venous malformation and lobar collapse
121
What is hypoxic pulmonary vasoconstriction?
When there is low oxygen in the lung the blood vessels constrict.
122
what are diseases of pulmonary circulation.
Pulmonary embolism, pulmonary hypertention pulmonary AVM
123
Where does the lung develop from?
the foregut ventral outpouching in the 5th week
124
What happens between 5-17 weeks in the lungs?
major exocrine gland, major structural units formed, angiogenesis lung fluid is looking like a secretory gland
125
What happens after 17 weeks to 25 weeks?
Canalicular phase, there is development of the distal architechture and the blood vessels form capillary bed.
126
What happens upto birth?
get alveolar sacs develop two types for cells.
127
when does lung development stop?
At about 5 years old
128
What can go wrong in embryonic stage of lung development?
fistula between trachea and oesophagus, lung dvelopment of one lung due to stenosis
129
What can go wrong in canalicular stage?
if blood supply doesn't develop well, also problems with alveolus and capillary. acinar prolems
130
What is the most common problem in premature babies in terms of lung development?
the alveolus is not properly developed and doesn't function very well
131
What is oxygen in the pulmonary circulation?
it is a vasodilator and so in lungs blood chases oxygen.
132
What happens in foetal lungs?
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
133
What is 123 in foetal circulation?
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
134
What happens after birth?
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.
135
What can go wrong after baby is born?
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
136
What happens in the alveolus after birth?
After birth the lungs begin to absorb the fluid very quickly to allow for gas exchange. this switch is from a secretory channel.
137
What is Laplace's law?
Pressure= 2T/radius
more pressure required to inflate a small sphere. surface tension tries to colapse the lungs the surfactant changes this.
138
What is surfactant?
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.
139
What are problems relating to surfactants?
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.
140
What is the name of the classification system of immune responses?
Gel and coumbs
141
What are cytokines?
Proteins that allow leukocytes and tissue cells to talk to eachother
142
Where do antigen presenting cells go?
to the lymph nodes
143
When are IgM antibodies made?
at the beginning of an infection
144
What are IgG?
highly specific that targed specific epitopes
145
What are Ig E?
Made to things we are allergic to and could be involved in response to parasites.
146
Where can IgA be found?
It can be found in mucous membranes
147
Outline the Gell and coombs classifications
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
148
Describe Type 1 reactions immune
Immunological memory to something causing an allergic response. Acute anaphalaxis, hayfevere and asthma
149
What is Atopy?
inherited tendency to exaggerated IgE response to an antigen.
150
What is anaphalaxis usually linked with?
IgE and histamine attaching to mast cells
151
How is atopy diagnosed?
Skin prick tests, RAST radio
152
What is goodpasture's syndrome?
A type 2 teactio where there are antibodies to basement membranes. Follows a viral infection sometimes. teatment to remove antibodies.
153
What are some common drug causes of hypersensitivity
Nitrofurantoin, Aminodarone, bleomycin, methotrexate, NSAIDs Immunoglobulin based treatements
154
What are some common lung diseases that are genetically linked?
Cystic fibrosis, Alpha-1 antitrypsin deficiency
155
How do genetics and disease presentation link?
Rare alleles caue the most sever disease more common cause things like COPD
156
at what age is it likelt that your lungs stop growing?
around 19/20 steepest growth is after 10 years
157
At what age is it expected that lung function peaks?
At around 20-25 years old
158
What is Cystic fibrosis?
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.
159
Describe the genetics of Cystic fibrosis.
most common lethal autosomal recessive genetic disorder in caucasions, Chromosome 7 defect in CFTR protein, 1600 mutations associated.
160
What does the CFTR protein do?
It transports chloride ions out of the cell. this helps with epithelial fluid managment includes lung and GI usually
161
What does the treatment of CF include?
Rescue when exacerbations occur, prevention or maintenance treatment
162
Explain rescue care in CF
2 week iv antibiotics can be done at home or hospital but can cause allergies renal impairment resistance and vein access problems
163
What does CF prevention management include?
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
164
What are/could be the applications of personalised medicine for CF
The fact one specific gene is affected is important and helpful. it has clear therapeutic targets and there can be directed genotype therapies developed.
165
What are some of the genotype directed therapies of CF?
Small molecule ganets facilitate CFTR processing (Ivacaftor) Orkambi mixed outcomes gene therapy nees more work on delivery of the drug
166
What is alpha-1 antitrypsin deficiency?
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.
167
Why is PaCO2 more important?
can change the pH of the blood which is not really wanted.
168
Which are the inputs to the brain involved with breathing?
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.
169
What are the areas of the brainstem that are involved with respiratory control?
pneumotaxic and apneustic centres in the pons, dorsal and ventral respiratory group in the medulla.
170
What do the Pneumotaxic and apneustic centre do?
it slows down or inhibits inspiration. and the apneustic moderates the pneumotaxic
171
What is the function of the dorsal and ventral respiratory groups?
dorsal is mainly active in inspiration. ventral is uses in both inspiration and expiration.
172
What is the central pattern generator?
It is located withing DRV VRG it starts and stops and resets the ventilatory drive.
173
What percentage of influence in central and peripheral does PaCO2 have?
central 60%, peripheral40%.
174
What is the primary influence in central chemo receptors?
PaCO2in carotids it is PaCO2 and PaO2 and pH.
175
Where are the central chemoreceptors?
in the pontomedullary junction.
176
Why are central chemoreceptors more sensitive to PaCO2 than H+
Hydrogen ions cannot pass across theblood brain barrier . whereas CO2 can
177
In the brain how are CO2 levels sensed?
By the H+ concentration from carbonic anhydrase,
178
Where are the carotid and aortic bodies?
bifurcation of common carotid, IX cranial nerve afferents, asending aorta and has vagal nerve afferents.
179
Whats the main sensor of oxygen?
the peripheral chemoreceptors not active across all PaO2 type 1 can release neurotransmitter when hypoxia.
180
What do stretch receptors do in the lung?
Sense lung volume for slowly adapting and fast adapting the smooth muscle of conducting airways.
181
What are irritant receptors like?
irritant receptors are in conducting airways and do gasp or cough reception,
182
What are J receptors?
Juxtapulmonary capillary the have C fibres
183
Where are some other receptors?
Nose nasopharynx and larynx. There are chemo and mechano receptors.
184
what are the muscle proprioceptors?
In the joints tendons and muscle spindle receptors in the intercostal muscles and the diaphragm.
185
What happens as you walk up a mountain?
PiO2 is reduced Fraction of O2 staysthe same. then alveolare oxygen reduces so arterial oxygen drops and therefor ventilation is increased.
186
What does ACID stand for and mean?
Gell and coombs
A – allergic
C – cytotoxic killing
I – immune complexes
D – delayed T helper cells
187
What happens in oxygen content of air in height?
the pecentage stays the same, but the pressure of oxygen would be lower in proportion to others.
188
What is intersting about oxygen pressure changes?
It changes the saturation of haemoglobin but not in a linear way.
189
What happens to body at high altitude?
Increased ventilation, lowers PaCO2 alkalotic and get thachycardia, with time this is reduce and the alkalosis is compensated by renal bicarbonate.
190
What are the three common altitude problems?
Acute mountain sickness, High altitude pulmonary Oedema and High altitude Cerebral Oedema.
191
What is Acute mountain sickness?
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
What is the cause of high altitude pulmonary oedema?
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
What is high altitude cerebreal oedema?
Serious Confusion behaviour change,
With Immediate descent, symptoms can resolve relatively quickly.
194
What can be done for people flying?
give oxygen
195
What is 10m of sea water equivalent to in pressure?
10m= 1ATM
196
What is boyles law?
P1V1=P2V1 when you change the volume the pressure changes and when you change the pressure the volume changes.
197
what happened in apnoea diving?(breath hold)
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
What is shallow water death?
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
What is the diving reflex?
stop breathing, bradycardia and peripheral vasoconstriction happens when cold water goes on the face
200
What does SCUBA stand for?
Self-contained underwater breathing apparatus.
201
What has to be considered with the gas canisters?
what ambient pressure you will be breathing the gas at.
202
What is Dalton's Law?
Each gas's partial pressure adds to the total pressure.
203
What is pulmonary oxygen toxicity?
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
How can you assess CNS oxygen toxicity?
VENTID
Vision
Ears(tinitus)
Nausea
Twitching
Irritability
Dizziness
Convulsions
205
What is inert gas narcosis?
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
What is decompression illness?
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
What is an arterial gas embolism?
Gas enters the circulation via a torn pulmonary vein. small pressure can can lead to arterial gas embolysm need recompression
208
What is pulmonary barotrauma?
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
What can cause lung problems?
Allergens Infection.
210
What is asthma?
Chronic inflamatory disease inflamationin the airways.
211
What are causes of asthma?
Environmental influences are important- pollens infectious agents fungi pets
Occupational- flour car spray paint resins cleaning agents laboratory animal workers wood dust.
212
What is the epedemiology of asthma?
5-16% have it wide variation between countries. Increased prevalence second half of 20th centurey often found in poorer individuals.
213
What is hypersensitivity pneumonitis?
Acute sub acute and chronic forms, immue complex related disease It is inflamation of the lung. IgG mediated significant environmental influences.
214
What are occupational causes of COPD?
Silica Coal Grain Cotton Cadmium less common PAH Isocyanates steel/iron processing. Agricultural dust, Biomass fuels. wood dust
215
What is the initial innate immune response to pathogens?
lt reacts quickly but in the same way each time
216
What is the adaptive immune response like?
It reacts slowly on first infection but due to its memory it can react to secondary infections faster
217
What is an antigen?
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
Which cells are antigen presenting cells?
Dendritic and monocyte/ macrophages. when they meet a foreign molecule they ingest it and digest then display these cells on its surface.
219
What are the two types of lymphocytes and what do they do?
T cells- secret cytokines, cytotoxicity and regulate immunity
B cells- release antibodies(immunoglobulins)
220
What are the properties of adaptive immunity?
Ability to mount highly specific responses to a range of antigens, self-tolerance, and developing some form of a memory
221
how do lymphocytes recognise specific antigens?
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
What is VDJ variety
During developement all but one V D and J versions are deleted and put into the RNA that forms many combinations.
223
What happens when an antigen recognised?
There is prolieration of that cell and this is very prone to mutation which allows more varaiability and this allows for evolution.
224
What is tolerance in immuity?
It is a state of unresponsiveness of the immune systen to antigens that would normally elicit an adaptive immune response.
225
Why is tolerance to self needed?
To stop auto immune responses being devloped and in pregnancy.
226
What is central tolerance?
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
What is peripheral tolerance?
when Tregs in lymphoid tissue suppress or delete lymphocytes that recognise the self antigens as foreign
228
How is immunological memory developed?
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
How are antigen presenting cells not phagoytosed themselves?
they display the antigen with major histocompatibility complex that shows that the cell is self (Human leukocyte antigen)
230
What happens if a nieve cytotoxic cell meets an antigen presenting cell?
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
What happens when a helper T cell meets an antigen presenting cell?
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
How does a B cell begin its role?
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
What is an IgM ?
immature plasma cells secrete it and happens in early response. the constant regions are not very available.
234
What do IgA do?
dimer that can accesss mucosal surfaces and mediates mucosal immunity
235
What to IgG and IgE do?
IgG are in circulation and activate phagocytosis, IgE bind to mast cells and mediates allergic reactions.
236
What are some of the effects of antibodies?
Neutralisation, agglutination(joining together), opsonization allowing phagocytosis, complement fixation constant and directly kills it
237
How is the immune response harnessed in vaccinations?
They stimulate the body to produce a response without the exposure to the pathogen.
238
What happens with reduced b cell function?
failure to eliminate pathogens such as bacteria specifically ones which have a waxy capsule. this recurrent infecion can cause scars in the lungs
239
What happens with failure of T cell immunity?
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
How does HIV act?
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
What happens in failed tolerance?
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
What is rheumatoid arthritis?
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
What is ANCA vasulitis?
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
How does chronic inflammation occur?
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
What are the three patterns of chronic inflamation?
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
Example of suppurative infalmation
lung abscesses , could be caused by and organism could be caused by obstruction tissue damage or be impaired immune system
247
What happens to rheumatoid dammage in thelung?
Repeated endothelial injury and leads to laying down of collagen and stops diffusion of oxygen, and leads to breathlessness
248
What is granulomatous inflamation?
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
What are the consequences of chronic inflamation?
Systemic problems
malais
weight loss
fever
anaemia
Tissue destruction
cavity formation
Fibrosis
growth disorders like cancers.
250
What is the treatment for chronic inflamation.
Treat the cause like infection or obstruction and immunosupressant drugs or NSAIDs
251
What does the parasympathetic nervous system do to the lungs?
Constricts bronchi
252
What does the sympathetic nervous system do to the lungs?
It dilates the bronchi
253
What causes bronchoconstriction?
Parasympathetic nervous sytem
254
What neurotransmitters are involved with bronchoconstriction/
Acetyl choline at both synapses
255
What receptor causes bronchoconstriction?
ACh acting on M3 muscarinic receptors
256
What are the treatments for bronchoconstriction?
Anticholinergic, muscarinic antagonists
257
What receptor mediates smooth muscle relaxation?
Beta 2 adrenergic receptors
258
What is released in the sympathetic nervous system to mediate bronchodilation?
Noradrenaline
259
What are the types of adrenergic receptors?
Alpha and Beta,
260
What structures contribute to the respiratory pump?
Bones (ribs and sternum), muscles (diaphragm and intercostals), pleura, nerves.
261
What structures make up the conducting airways?
Nose, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles.
262
What is the function of the conducting airways?
To filter, warm, humidify and conduct air to the lungs.
263
What is respiratory epithelium?
Pseudo-stratified, columnar, ciliated, interspersed with goblet cells.
264
Where is the resistance greatest in the airway?
In the trachea - the trachea is longer (length adds resistance) and there is only one of it (branching decreases resistance).
265
What equation can be used to demonstrate resistance of an airway?
Poiseuille's law: R = 8ƞl / πr^4.(ƞ = viscosity, l = length).
266
Briefly describe inspiration.
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
What is the 'pump handle' representing?
The movement of the sternum. In inspiration the sternum moves anteriorly and superiorly.
268
What is the 'bucket handle' representing?
The movement of the rib cage. In inspiration the rib cage moves upwards and outwards.
269
Briefly describe expiration.
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
Which muscles are involved in active expiration?
The internal intercostals; these muscles contract pulling the ribcage inwards and downwards.
271
What is V/Q mismatch?
When the perfusion of blood in capillaries isn't matching the ventilation of the alveoli.
272
What is it called when you have a high V/Q ratio?
Dead space. Lots of ventilation but no perfusion.
273
What is a cause of a high V/Q ratio (dead space)?
Pulmonary embolism.
274
What is it called when you have a low V/Q ratio?
Shunt. Lots of perfusion but no ventilation.
275
What is a cause of a low V/Q ratio (shunt)?
Pulmonary oedema.
276
What is perfusion of pulmonary capillaries dependent on?
1. Pulmonary artery pressure.2. Pulmonary venous pressure.3. Alveolar pressure.
277
Does the apex of the lung have a high or a low V/Q? Why?
High - effect of gravity, far more perfusion at the base of the lung.
278
What are the 7 layers for gas exchange?
1. Alveolar epithelium. 2. Interstitial fluid.3. Capillary endothelium.4. Plasma layer.5. RBC membrane.6. RBC cytoplasm.7. Hb binding sites.
279
Name 4 causes of hypoxia.
1. Hypoventilation.2. V/Q mismatch.3. Diffusion abnormality.4. Reduced PiO2.
280
Name 4 causes of hypercapnia.
1. Increased dead space ventilation; rapid, shallow breathing. 2. V/Q mismatch.3. Increased CO2 production.4. Reduced minute ventilation.
281
What is the alveolar gas equation?
PAO2 = PiO2 - (PaCO2/R)
282
What is Dalton's law?
In a mixture of non reacting gases Ptotal = Pa + Pb. (P total is the sum of the pressures of individual gases).
283
What is Boyle's law?
Pressure and Volume are inversely proportional:P1V1 = P2V2.
284
What is Henry's law?
The solubility of a gas is proportional to the partial pressure of the gas. S1/P1 = S2/P2.
285
What is the acid/base dissociation equation?
CO2 + H2O = H2CO3 = HCO3- + H+
286
What enzyme catalyses the formation of bicarbonate and hydrogen ions from CO2 and H2O?
Carbonic anhydrase.
287
What is the henderson hasselbalch equation?
pH = pKa + log (A-)/(HA)
288
What is Laplace's law?
P = 2T/R.
289
What is the significance of Laplace's law?
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
Where is surfactant produced?
It is produced by type 2 pneumocytes in the alveoli.
291
When is surfactant produced?
It starts being produced from 34 weeks gestation and production increases rapidly 2 weeks before birth.
292
List 4 functions of surfactant.
1. Prevents alveoli collapse.2. Allows homogenous aeration.3. Reduces surface tension.4. Maintains functional residual capacity.
293
Premature babies may have surfactant deficiency. What are the consequences of this?
1. Respiratory distress syndrome.2. Non-compliant lungs.3. Unequal aeration.4. Reduced lung volume.
294
How can you treat surfactant deficiency?
Ensure the patient is warm and is receiving O2 and fluids. Begin surfactant replacement.
295
Briefly describe the controller-effector-sensor loop.
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
What does the pneumotaxic area do and where is it located?
It switches off inspiratory neurones and so allows expiration. It is located in the upper pons.
297
What does the apneustic centre do and where is it located?
It inhibits expiration by activation inspiratory neurones. It is located in the lower pons.
298
Where are SASR (slow adapting stretch receptors) located?
Found in smooth muscle around airways.
299
What activates SASR?
Lung distension.
300
How do SASR respond to activation?
They inhibit inspiration and so promote expiration.
301
Where are RASR (rapidly adapting stretch receptors) located?
Between airway epithelial cells.
302
What activates RASR?
Lung distension and irritants.
303
How do RASR respond to activation?
Bronchoconstriction.
304
What activates C fibres J receptors?
Increased interstitial fluid volume.
305
How do C fibres J receptors respond to activation?
They cause rapid, shallowing breathing. Bronchoconstriction and cardiovascular depression.
306
Where are central chemoreceptors located?
Medulla oblangata.
307
What stimulates central chemoreceptors?
An increase in H+ concentration in the ECF.
308
Where are peripheral chemoreceptors located?
Carotid and aortic bodies.
309
What stimulates peripheral chemoreceptors?
A decrease in PaO2.
310
What is the respiratory drive more senstitive to, CO2 or O2?
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
Oxygen dissociation curve: what causes the curve to shift to the right?
An increase in temperature and a decrease in pH.
312
Oxygen dissociation curve: what does it mean when the curve shifts to the right?
There is increased O2 unloading. Hb's affinity for oxygen has decreased.
313
Oxygen dissociation curve: what causes the curve to shift to the left?
A decrease in temperature and an increase in pH.
314
What is a cause of respiratory acidosis?
Inadequate ventilation; could be due to obstruction e.g. COPD.
315
What is the renal compensation mechanism for respiratory acidosis?
Increased ammonia formation. H+ secretion increases and there is increased HCO3- reabsorption.
316
What can cause respiratory alkalosis?
Hyperventilation in response to hypoxia.
317
What is the renal compensation mechanism for respiratory alkalosis?
H+ secretion decreases; more H+ is retained. HCO3- secretion.
318
What is a cause of metabolic acidosis?
Renal failure; loss of HCO3-, excess H+ production.
319
What is the respiratory compensation mechanism for metabolic acidosis?
Chemoreceptors stimulated, enhancing respiration, PaCO2 decreases.
320
What is the respiratory compensation mechanism for metabolic alkalosis?
Chemoreceptors are inhibited, reduced respiration, PaCO2 increases.
321
What is a cause of metabolic alkalosis?
Vomiting; loss of H+.
322
Is respiratory compensation fast or slow?
FAST!
323
What is type 1 respiratory failure and what are its causes?
Hypoxemia. Causes: V/Q mismatch due to alveolar hypoventilation, high altitude, shunt, diffusion problem.
324
What is type 2 respiratory failure and what are its causes?
Hypoxemia and hypercapnia. Causes: inadequate alveolar ventilation due to reduced breathing effort, decreased SA, neuromuscular problems.
325
What is forced vital capacity?
Volume of air that can be forcibly exhaled after maximum inhalation.
326
How could you diagnose a patient with having an obstructive lung disease?
The FEV1/FVC ratio would be less than 70% predicted value.
327
How could you diagnose a patient with having an restrictive lung disease?
The FEV1/FVC ratio would be normal but their FVC value would be very low.
328
How can you work out total lung capacity?
Add vital capacity to residual volume.
329
What is tidal volume?
The volume of air moved into or out of the lungs during normal, quiet breathing.
330
What changes are seen in an aging lung?
Decreased compliance, muscle strength, elastic recoil, immune function. Decreased response to hypoxia and hypercapnia. Impaired gaseous exchange.
331
What happens to the FEV1 and FVC in an elderly person?
They both decrease and the residual volume increases.
332
What effect does hypoxia have on pulmonary vessels?
It vasoconstricts the vessels and so redirects blood to O2 rich alveoli.
333
What is hypersensitivity?
Undesirable reaction produced by the immune system.
334
Hypersensitivity: What is the mechanism of a type 1 reaction?
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
What is the parasympathetic neurotransmitter in the lungs?
Acetylcholine.
336
What is the sympathetic neurotransmitter in the lungs?
Noradrenaline.
337
What is the effect of Ach on the pulmonary vessels?
Bronchoconstriction and vasodilation.
338
What is the effect of noradrenaline on the pulmonary vessels?
Bronchodilation and vasoconstriction.
339
Name 2 receptors for Ach.
Muscarinic (G protein coupled) and Nicotinic (ligand gated ion channels).
340
Host defense: What is innate immunity?
Immunity that doesn't require prior exposure. It usually involves phagocytosis and inflammation.
341
Briefly describe the mechanism of inflammation.
Vasodilation results in exudation of plasma. Neutrophils and monocytes migrate into tissues.
342
What are alveolar macrophages derived from?
Monocytes. They are the resident phagocyte in the lungs and they coordinate inflammatory response.
343
What is the function of the epithelial barrier in host defense?
Moistens and protects airways. Functions as a barrier to pathogens and foreign matter.
344
What is the muco-ciliary escalator?
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
What is coughing?
An explosive expiration that acts to clear foreign matter from the airways. It is an important defense mechanism.
346
What does the lung bud form from?
The respiratory diverticulum - an out-pouching of the fore gut.
347
What is the septum called that seperates the lung bud from the oesophagus in the embryo?
Tracheoesophageal septum.
348
What are the 5 stages of respiratory tract development called? What happens in these stages?
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
Describe the first breath.
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
Define anatomical dead space.
The volume of air taken in during a breath that does not enter the alveoli.
351
Define physiological dead space.
The volume of air that is taken in during a breath that does not take part in gas exchange.
352
What it total lung capacity equal to?
TLC = VC + RV.
353
Where is the basic neural machinery for the generation of the respiratory rhythm located?
In the lower medulla.
354
True or False: the intercostals are the main muscles of respiration.
False - the diaphragm is the main muscle of respiration.
355
Which alveoli are preferentially ventilated and perfused?
Those at the base of the lungs.
356
Why can hypoxia cause respiratory alkalosis?
Hypoxia leads to hyperventilation as the person tries to inhale more O2. This means you lose a lot of CO2 resulting in alkalosis.
357
Define total lung capacity.
The vital capacity plus the residual volume. It is the maximum amount the lungs can hold.
358
Define residual volume (RV).
The volume of air remaining in the lungs after a maximal exhalation.
359
Define functional residual capacity (FRC).
The volume of air remaining in the lungs after a tidal volume exhalation.
360
Define tidal volume (TV).
The volume of air moved in and out of the lungs during a normal breath.
361
Define FEV1.
The volume of air that can be forcibly exhaled in 1 second.
362
What 2 equations can be used to work out TLC?
1. TLC = VC + RV.2. TLC = TV + FRC + IRV.
363
Define forced vital capacity (FVC).
The maximum volume of air that can be forcibly exhaled after maximal inhalation. Usually in 6 seconds.
364
Define expiratory reserve volume (ERV).
The additional volume of air that can be forcibly exhaled after a tidal volume expiration.
365
Define inspiratory reserve volume (IRV).
The additional volume of air that can be forcibly inhaled after a tidal volume inspiration.
366
What is lung compliance?
A measure of the lung's ability to stretch and expand. Compliance = ∆V/∆P.
367
Why do you see decreased elastic recoil in an ageing lung?
The elastin degenerates and ruptures.
368
Why do you see decreased muscle strength in an ageing lung?
There is a decrease in type 1, fatigue resistant fibres. And muscle mass also decreases.
369
Why do you see a decreased response to hypoxia and hypercapnia in an ageing lung?
The lung is more vulnerable and has a decreased awareness meaning these changes aren't detected till late on.
370
Why do you see decreased immune function in an ageing lung?
There is less protective mucus and sputum clearance is less effective.
371
Why do you see impaired gaseous exchange in an ageing lung?
The SA for gaseous exchange decreases and there is increased V/Q mismatch.
372
Why does the residual volume increase in an ageing lung?
The chest wall changes shape. There is increased calcification and stiffness.
373
What is the main cell involved in acute inflammation?
Neutrophils.
374
What can the pneumotaxic area override?
The apneustic area.
375
Name 4 non-immune host defense mechanisms.
1. Mucus.2. Muco-cilliary escalator.3. Epithelium.4. Cough.
376
What layer of the tri-laminar disc is the respiratory tract derived from?
The endoderm.
377
What is the respiratory diverticulum an out-pouching of?
The foregut.
378
What does the respiratory diverticulum go on to form?
The lung buds.
379
Give 2 ways that oxygen is carried around the body?
1. Bound to Hb.2. Dissolved in blood.
380
What is Hb affinity for O2?
How readily Hb acquires and releases O2 at respiring tissues.
381
Does the umbilical vein carry oxygenated blood or deoxygenated?
Oxygenated (umbilical artery carries deoxygenated).
382
What is the importance of the ductus venosus in foetal circulation?
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
Define vital capacity.
The maximum volume of air that can be exhaled after a maximal inhalation.
384
What is the normal tidal volume in an adult?
500ml.
385
What cell type lines most of the surface of an alveoli?
Type 1 pneumocytes. Type 2 are more numerous but type 1 are squamous and so are responsible for more of the SA.
386
What is the thickness of the air-blood barrier in nm?
200-800 nm.
387
What is the epithelium of the vocal cords?
Stratified squamous non-keratinising.
388
What is the base, apex and roof of the maxillary sinus formed from?
Base - lateral wall of the nose. Apex - zygomatic process of the maxilla. Roof - floor of the orbit.
389
Which sinus is a labyrinth of air cells?
The ethmoid.
390
What vertebral level does the larynx extend to?
C6.
391
True or False: alveolar macrophages release interleukins.
True - this is important in the coordination of an immune response.
392
Why does constriction of bronchioles cause significant increase in airway resistance and can cause an expiratory wheeze such as seen in asthma?
Bronchioles have no cartilage, only smooth muscle. This means they are more likely to constrict and increase airway resistance.
393
Which respiratory tract structures are lined with smooth muscle and contain no cartilage?
Bronchioles.
394
Define peak expiratory flow (PEF).
The greatest rate of airflow that can be obtained during forced exhalation.
395
Define airway obstruction.
Impediment to inspiratory and expiratory air flow.
396
Define airway restriction.
When the lungs are restricted from full expansion.
397
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.
IgE
Mast Cell
Histamine
398
What are broncho-pulmonary segments?
Discrete functional and anatomical units of the lung. Each segment is supplied by a specific segmental/tertiary bronchus.
399
How many broncho-pulmonary segments are there in the right lung?
10
400
How many broncho-pulmonary segments are there in the left lung?
8
401
What effect does hypoxia have on systemic vessels?
Vasodilation.
402
How do we recognise pathogens we have nerve seen before?
Pattern recognition receptors - PRRs.
403
What are the causative agents of acute inflammation?
Pathogens, damaged tissue.
404
What are the causative agents of chronic inflammation?
Persistent acute inflammation, persistent foreign bodies, autoimmune reactions.
405
What are main cells involved in acute inflammation?
Neutrophils! Also eosinophils and basophils.
406
What are main cells involved in chronic inflammation?
Mononuclear cells e.g. monocytes, macrophages, lymphocytes, plasma cells.
407
What are the primary mediators in acute inflammation?
Vasoactive amines.
408
What are the primary mediators in chronic inflammation?
Cytokines, growth factors, ROS etc.
409
What are the outcomes of chronic inflammation?
Tissue destruction, fibrosis, necrosis, chronic inflammation.
410
What are the outcomes of acute inflammation?
Resolution.
411
What suppresses alveolar macrophage activation in a healthy lung?
Respiratory epithelium.
412
Which results in inflammation, necrosis or apoptosis?
Necrosis.
413
Why is the lung at increased risk of inflammation?
1. Huge area in contact with the external environment.2. The lung contains the majority of our WBC's at any one time.
414
What is the function of mucus?
It protects the epithelium from foreign material and from fluid loss.
415
What mechanism moves airway mucus up into the throat?
Muco-ciliary escalator.
416
What is mucus composed of?
Water, carbohydrates, lipids and proteins.
417
Name 4 non-immune host defence mechanisms.
1. Epithelial barrier. 2. Mucus. 3. Muco-ciliary escalator. 4. Coughing.
418
What nerves does the efferent limb of the cough reflex include?
Recurrent laryngeal and spinal nerves.
419
What nerves does the afferent limb of the cough reflex include?
Receptors within the sensory distributions of Cn 5, 9 and 10.
420
What is adaptive immunity?
An antigen-specific immune response.
421
What is the function of B cells?
Antibody production.
422
Name 3 types of T cells.
1. Cytotoxic T cells. 2. Helper T cells. 3. Memory T cells.
423
What is the function of cytotoxic T cells?
They track down infected cells.
424
What is the function of helper T cells?
they secrete cytokines to attract macrophages and neutrophils etc.
425
What can cause a type 1 hypersensitivity reaction?
Pollen, cat hair, peanuts (allergies).
426
What can cause a type 2 hypersensitivity reaction?
Transplant rejection, transfusion mismatch.
427
What can cause a type 3 hypersensitivity reaction?
Fungal.
428
What can cause a type 4 hypersensitivity reaction?
TB.
429
What are the functions of lymphocytes?
They make antibodies, decide what type of antibodies to make and kill diseased cells.
430
What is the Gell and Coombs classification?
It describes 4 types of hypersensitivity reaction.
431
Describe the mechanism and give examples of a type 1 hypersensitivity reaction.
- 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
Describe the mechanism and give examples of a type 2 hypersensitivity reaction.
#NAME?
433
Describe the mechanism and give examples of a type 3 hypersensitivity reaction.
- Mechanism: immune complexes, activation of complement. - Fungi and pigeon droppings etc. (pigeon fancier's lung).
434
Describe the mechanism and give examples of a type 4 hypersensitivity reaction.
#NAME?
435
What comprises a respiratory acinus?
Respiratory bronchiole, alveolar duct and alveolus.
436
What part of the respiratory tract lies behind the sternal angle?
The tracheal bifurcation.
437
Give an example of a restrictive lung disease?
Pulmonary fibrosis.
438
Give an example of an obstructive lung disease?
Chronic bronchitis and emphysema.
439
What is the affect of pulmonary fibrosis on the following: FEV1, FVC, PEF, TLC and DLCO?
All reduced except PEF which is non variable
440
What is the affect of emphysema on the following: FEV1, FVC, PEF, TLC and DLCO?
- FEV1 = reduced. - FVC = normal or slightly reduced. - PEF = typically not variable. - TLC = increased (hyperinflation). - DLCO = reduced.
441
What is the affect of asthma on the following: FEV1, FVC, PEF, TLC and DLCO?
#NAME?
442
What is DLCO?
Uptake of CO in ml at standard temperature and pressure.
443
Define inspiratory capacity (IC).
The maximum volume of air that can be forcibly inspired - IC = TV + IRV.
444
What are the 6 stages of neutrophil action?
1. Identify threat.2. Activation. 3. Adhesion. 4. Migration. 5. Phagocytosis. 6. Bacterial killing.
445
What is the consequence of mucus plugs in the lungs?
Airway obstruction which can ultimately lead to death.
446
What is the equation for trans-pulmonary pressure?
Transpulmonary pressure = alveolar pressure - pleural pressure. (TPP is always positive).
447
What layer of the trilaminar disc is pleura derived from?
Mesoderm.
