Respiratory Flashcards

Question

What happens to the intercostal muscles, diaphragm, volume and pressure during inspiration and expiration?

Answer 1

- Inspiration: - Intercostal muscles = contract - Diaphragm = contract - Volume = increases - Pressure = decreases, so air moves in - Expiration: - Intercostal muscles = relaxes - Diaphragm = relaxes - Volume = decreases - Pressure = increases, so air moves out

Answer 2

- It is the volume of inspired air that is not contributing to ventilation. There is anatomical (due to anatomy), that makes up more ml, and alveolar. So, the physiological deadspace = anatomical + alveolar

Answer 3

- O2 in, CO2 out - 1000 capillaries per alveolus, each erythrocyte may come into contact with multiple alveoli - Capillaries at most dependent parts of lung are preferentially perfused with blood at rest - Perfusion of capillaries with oxygen depends on pulmonary artery pressure, pulmonary venous pressure etc. - Hypoxia = where region of body deprived of oxygen. Pulmonary vasoconstriction diverts blood to better-oxygenated lung segments, thereby optimising ventilation/perfusion matching + system oxygen delivery

Answer 4

- Arterial O2/CO2 - Alveolar O2/CO2 - Pressure of inspired O2 - Alveolar ventilation - CO2 production

Answer 5

- CO2 elimination: PaCO2 = k V'CO2/V'A - Three ways CO2 is carried: - Bound to haemoglobin - Plasma dissolved - As carbonic acid - Physiological causes of high CO2: - V'A reduced = either reduced minute ventilation, increased deadspace ventilation by rapid shallow breathing or increased deadspace ventilation by ventilation/perfusion mismatching - Increased CO2 production

Answer 6

- Alveolar gas equation: PAO2 = Pi02 - PaCO2/R (R is respiratory quotient) - Causes of low PaO2 (hypoxaemia): - alveolar hyperventilation - reduced PiO2 - ventilation/perfusion mismatching - diffusion abnormality

Answer 7

- pH needs to be maintained to ensure optimal function - CO2 elimination from the lungs is one mechanism to maintain pH - Carbonic acid equilibrium = CO2 + H2O \<-\> H2CO3 \<-\> H+ + HCO3- - HCO3- = weak base - H2CO3 = weak acid

Answer 8

- Henderson-Hasselbach equation: pH = 6.1 + log10((HCO3-) / (0.03 x PaCO2) ) - 4 main acid base disorders: - Respiratory acidosis = increased PaCO2, decreased pH, mild increased HCO3- - Respiratory alkalosis = decreased PaCO2, increased pH, mild decreased HCO3- - Metabolic acidosis = reduced bicarbonate + decreased pH - Metabolic alkalosis = increased bicarbonate + increased pH

Answer 9

Physical, chemical + cellular defences that aim to immediately prevent the spread of foreign pathogens

Answer 10

Initiated by tissues, epithelial production of hydrogen peroxide + release of cellular contents. Amplified by specialist macrophages, e.g. Kupffer cells, alveolar

Answer 11

Provides defence against infection + hostile environment but many will die of diseases caused by inflammatory processes, e.g. COPD

Answer 12

Pattern recognition receptors, e.g. toll-like receptors

Answer 13

Dendritic cells, Kupffer cells (liver), histiocytes + alveolar macrophages. They initiate acute inflammation via cytokines + antigen presentation

Answer 14

- Neutrophils comprise 70% of leukocytes - Contain primary granules (myeloperoxidase, elastase etc.) + secondary granules (receptors, lysozyme etc.) - Carry our bacterial killing through enzyme release (order): - Identify threat - receptors - Activation - Adhesion - Migration - Phagocytosis (membrane invagination + pinching PHAGOSOME (vesicles around particle), fusion with granules PHAGOLYSOSOME (fusion of phagosome + lysosome) - Bacterial killing - Apoptosis (need to get rid of them after use)

Answer 15

Yes, it can contract + relax to regulate airway diameter

Answer 16

- Regulated by autonomic nervous system (contractile signals cause increase in intracellular calcium in smooth muscle, which activated actin-myosin contraction) - Regulated by inflammation

Answer 17

- Autonomic nervous system conveys all outputs from CNS to body, except for skeletal muscle control - Two nerves in series, pre- + post- ganglionic fibres. Parasympathetic ganglia are near their targets with short post-ganglionic nerves, whereas sympathetic ganglia are near spinal cord with long post-ganglionic fibres

Answer 18

- Parasympathetic nervous system - Vagus nerve neurons terminate in parasympathetic ganglia in airway - Short post-synaptic fibres reach muscle + release acetylcholine, which acts on receptors to stimulate airway smooth muscle contraction - Excessive bronchoconstriction = bad, inhibition of parasympathetic nervous system beneficial (drugs block M3 receptor = anti-cholinergics or anti-muscarinics (can be short-acting or long-acting muscarinic antagonists). Beta agonists engage them, anti-muscarinics oppose them

Answer 19

- Nerve fibres release noradrenaline which activates adrenergic receptors on airway smooth muscles, causes muscle relaxation

Answer 20

- Binds to beta-2 receptor, ATP turned to cAMP, this converts inactive protein kinase to activated protein kinase = muscle relaxation - Raising cAMP may activate Na/K exchange pump driving influx of potassium - Tachychardia

Answer 21

- Particle size (main factor) - Flow rate - Underlying disease - Device

Answer 22

- Innate = induced by infection, e.g. cytokines, macrophages. Initial response - Adaptive = specific to pathogen, happen later + generate 'memory' with a learned response that is more rapid and effective - This happens throughout the respiratory tract + involves epithelium

Answer 23

- Functions as a barrier to pathogens and contains mucosal glands - mucociliary escalator

Answer 24

- Antiproteinases (lysozymes) - Anti-fungal proteins - Anti-microbial proteins (a&b defensins) - Surfactants (A&D)

Answer 25

Mucus + products of submucosal glands. Coughing + sneezing are significant non-immune defence mechanisms

Answer 26

Secretory product of mucous cells (goblet cells of airway surface epithelium + submucosal glands), vasoelastic gel. Protects epithelium from foreign material + fluid loss, transported from lower respiratory tract into pharynx by air flow + mucociliary clearance. Cilia beat in directional waves to move mucus up the airways

Answer 27

- Coughing = expulsive reflux with some voluntary control, clearance of irritants - Sneezing - involuntary reflex in response to nasal muscosa irritation or excess fluid in airway

Answer 28

- Yes. Airway epithelium exhibits level of plasticity. The multipotential basal cell population can differentiate into respiratory epithelium if damage occurs - Abnormal epithelial responses to injury underpin many obstructive lung diseases

Answer 29

- Inspiratory Reserve Volume (IRV) = max. inhalation of tidal (normal) breathing = 2000ml - Expiratory Reserve Volume (ERV) = max. inhalation of tidal (normal) exhalation = 1250ml - Residual Volume (RV) = air in lungs after max. expiration; keeps alveoli inflated between breaths + mixes with fresh air on next inspiration = 1250ml - Vital Capacity (VC) = amount of air that can be exhaled with maximum effort after maximum inspiration (ERV + TV + IRV) = 3750ml - Functional Residual Capacity (FRC) = amount of air remaining in lungs after normal tidal expiration (RV + ERV) = 2500ml - Inspiration Capacity (IC) = max. inspiration after tidal (normal) expiration (TV + IRV) - Total Lung Capacity (TLC) = maximum amount of air the lungs can contain (RV + VC) = 5000ml - Tidal volume (TV) = amount of air inhaled or exhaled in one breath - 500ml a breath

Answer 30

- FEV1 is measured in a spirometry test. It is the volume of air that is forced out in one second after taking a deep breath - FVC (forces vital capacity) is the volume of air exhaled from lungs after taking the deepest breath possible, measured by spirometry - Divide FEV1/FVC to give a volume-time curve. Shows proportion of person's vital capacity that they are able to expire in first second of forced expiration to fill, forced vital capacity. Should be expelled in 6 seconds

Answer 31

- PEF = peak expiratory flow (rate). It is the single measure of the highest flow during expiration. Measured with a peak flow meter - Flow-volume loop from spirometry test is a plot of inspiratory + expiratory flow against volume. PEF = peak flow, FEF25 = flow at point when 25% of total volume to be exhaled has been exhaled

Answer 32

- Obstruction = blockage of airways. Eventually reach FVC. Asthma, COPD (learn) - Restriction = can't expand lungs, can't reach FVC. Obesity, pulmonary fibrosis (learn)

Answer 33

- Airway obstruction: - FEV1/FVC ratio = \<70%, low FEV1 (\<80%) - FVC = normal - Airway restriction: - FEV1/FVC ratio = \<80%, low FEV1 - FVC = \<80%

Answer 34

- Gas dilution - Body box (total body plethysmography) - RV and TLC can be calculated from the measurements, e.g. FRC, VC, expiratory reserve volume. TLC = VC + RV

Answer 35

DLCO is the diffusing capacity of lung for carbon monoxide. Carbon monoxide is used to estimate DLCO. Technique = hold breath for 10 seconds now with known amount of CO inhaled. Expired CO is measured. This is reduced with COPD

Answer 36

- Compliance of the lung = change in volume per unit change in pressure gradient between pleura and alveoli. Greater lung compliance = more readily the lungs are expanded - Determined by stretchability of lung tissues: a thickening + thus a loss in stretchability of the lung's elastic connective tissues results in a decrease in lung compliance - Static compliance (measured during breath-hold) + dynamic compliance (measured during regular breathing)

Answer 37

- Found in the pons of midbrain, control breathing - Apneustic centre: - Area of lower pons - Major source of input to medullary inspiratory neurons. Increase inspiratory intensity - Pneumotaxic centre: - Area of upper pons - Modulates activity of apneustic centre to allow for expiration, increased innervation leads to shallower ventilation with increased frequency

Answer 38

- Neural activity that controls contraction of diaphragm + intercostal muscles - Dorsal respiratory group (DRG): - Rapidly fire during inspiration - Input to spinal nerves that control diaphragm + inspiratory intercostals - Ventral respiratory group (VRG): - Pre-Botzinger complex of neurons located in upper part of VRG. This is where respiratory rhythm generator is - Sets respiratory basal rate - Neurons fire during both inspiration + expiration - Have input to muscles of inspiration - Lower VRG also contains expiratory neurons, input to muscles of expiration

Answer 39

- Inspiration: - Diaphragm stimulated to contract + flatten - Volume increases + pressure decreases (Boyle's law) - Chest wall moves away from lung surface + parietal pleura moves away from visceral slightly - Transpulmonary pressure (force acting to expand lungs) increases - Pressure enough to overcome elastic recoil - Lungs expand + air forced in - Expiration: - Relaxation, increasing pressure + elastic recoil forces air out

Answer 40

- Central chemoreceptors: - In medulla. Not within DRG/VRG complex - Provide excitatory synaptic input to medullary inspiratory neurons - Sensitive to PaCO2 of blood perfusing brain. Stimulated only by an increase in H+ concentration in ECF - Peripheral chemoreceptors: - Aortic bodies and carotid bodies - Stimulated by decrease in PaO2 and increase in arterial H+ concentration

Answer 41

Proportional to PaCO2 and 1/PaO2

Answer 42

- Control by PO2: - Decrease in PO2 stimulates peripheral chemoreceptors - Send impulses to medullary inspiratory neurons + cause increase in ventilation rate - Control by CO2: - Increase in PCO2 = increase in H+ in blood (CO2 + H2O -\> H+ + HCO3-) - Stimulates peripheral chemoreceptors + medullary inspiratory neurons - Increase in CO2 in brain ECF - H+ stimulates central chemoreceptors - Ventilation increased to remove excess CO2

Answer 43

- Mechanoreceptors - Slowly adapting stretch receptors (SASR): - In smooth muscle layer of airways in lungs - Stimulated by large lung inflation - Send afferent (afferent = arrives, efferent = exits) impulses to brain + inhibit medullary inspiratory neurons in DRG. Inhibit inspiration in response to stretch (Hering-Breuer reflex) - Rapidly adapting stretch receptors (RASR): - In-between epithelial cells of airways - Respond to rate of change in volume + irritants - Stimulation causes bronchoconstriction + activity burst - J receptors: - Stimulated by increase in lung interstitial pressure - Effects are rapid breathing, dry cough, sensation of pressure in chest + dyspnoea

Answer 44

- Nose, nasopharynx and larynx: - Chemo and mechano receptors, some appear to sense + monitor flow. Inhibit the central controller - Pharynx: - Receptors activated by swallowing, stops respiratory activity to protect against risk of aspiration of food or liquid

Answer 45

- Important roles in perception of breathing effort

Answer 46

- Hypoxia = deficiency of oxygen at the tissue level - Hypercapnia = increase in PCO2 in the arterial blood. Hypercapnia is the main drive to breathe

Answer 47

- Hypoxaemia = reduced PaO2 - Anaemia or CO hypoxia = when arterial PO2 isn't decreased total amount of O2 in blood is decreased due to lack of erythrocytes or abnormal erythrocytes - Ischaemic hypoxia = blood flow to tissues is too low - Histotoxic hypoxia = cells unable to utilise O2 delivered to them due to a toxic agent, e.g. cyanide

Answer 48

- Hypoventilation = resulting in increased arterial partial CO2 pressure. Failure to ventilate the alveoli adequately - Diffusion impairment = results from thickening of alveolar membranes or decrease in their SA. Causes blood partial O2 pressure + alveolar partial O2 pressure to fail to equilibriate - Shunting = abnormality that causes blood to flow from one circulatory system to another, e.g. oxygenated blood mixes with deoxygenated blood, so reduces overall pressure of O2. Right-to-left shunt allows deoxygenated systemic venous blood to bypass lungs + return to body - Ventilation-perfusion mismatch = most common cause of hypoxaemia. Air reaches entire lung but some areas aren't perfused so O2 can't get into blood via alveoli. There may be ventilated alveoli but no blood supply (dead space or wasted ventilation). There may be adequate blood flow but no ventilation (shunt)

Answer 49

- Respiratory failure = failure of gas exchange, inability to maintain normal blood gases. Either acute (rapid) or chronic (over time) - Type I: - PaO2 = low (hypoxia) - PaCO2 = low/normal (hypocapnia/normal) - Caused by problem with oxygenation, e.g. high altitude, shunting. Pulmonary embolism (form of ventilation-perfusion mismatch) most commonly causes Type I

Answer 50

- PaO2 = low (hypoxia) - PaCO2 = high (hypercapnia) - Caused by poor ventilation, e.g. COPD, asthma

Answer 51

PaO2 = PiO2 - PaCO2/R (respiratory quotient = ratio of volume of CO2 produced to volume of O2 used)

Answer 52

PaCO2 = 1/alveolar ventilation

Answer 53

- Type I = treat primary cause and give O2 - Type II = be careful when giving O2 as rely on hypoxia to stimulate respiration. They've got so used to high levels of CO2, so we must not take away their drive to breath

Answer 54

- Pulmonary circulation: - 100% of blood from right ventricle - 5 seconds transit time - Thin wall with little muscle to allow for rapid diffusion of gases - Lower blood pressure. Important as otherwise would damage thin walls between capillaries + alveolar spaces - Bronchial circulation: - Part of systemic circulation, 2% of output from left ventricle. Oxygenated blood supplying tissues - Thicker walls with significant muscle - Higher blood pressure

Answer 55

- Resistance = 8 x L x viscosity / pi r^4 - Main thing to know is that resistance is inversely proportional to vessel radius to power of 4. Therefore, relatively small increase in radius causes dramatic reduction in resistance

Answer 56

- mPAP - PAWP = CO x PVR - mPAP = mean pulmonary arterial pressure - PAWP = pulmonary arterial wedge pressure (just a measure of left atrial pressure) - CO = cardiac output - PVR = pulmonary vascular resistance - Essentially saying that pressure difference across pulmonary circulation = cardiac output x resistance - During exercise, cardiac output increases but pressure stays the same. This is because resistance decreases

Answer 57

a) VQ mismatch b) Increased PVR c) Shunt

Answer 58

- Embryonic (0-5 weeks) - Pseudoglandular phase (5-17 weeks) - Cannalicular phase (16-25 weeks) - Alveolar (25 weeks-term)

Answer 59

- Lungs develop from respiratory diverticulum, an outbranch of foregut. By 5th week, lung buds enlarge to form left + right main bronchi

Answer 60

- Development of conducting airways (5-17 weeks)

Answer 61

Capillaries, vasculature + alveoli form (16-25 weeks)

Answer 62

- Alveoli develop. They further develop after birth, up to age 5

Answer 63

Vasodilator, hypoxia is a vasoconstrictor. Opposite in systemic circulation

Answer 64

Remember 1, 2, 3: - Umbilical vein = oxygenated, from placenta to foetus - Two umbilical arteries = deoxygenated, from foetus to placenta - Three foetal shunts to bypass the lung: - Foramen ovale = connection between R + L atria to bypass pulmonary circulation so blood goes from RA to LA - Ductus venous = shunt blood in umbilical vein to inferior vena cava - Ductus arteriosus = connects pulmonary artery to aorta to skip circulation in lungs - Foramen ovale, ductus arteriosus close after birth

Answer 65

P = 2T/R = pressure within alveolus is directly proportional to surface tension + inversely proportional to radius. Smaller radius = higher surface tension

Answer 66

Surfactant, released by type II pneumocytes decreases the surface tension. This increases the stability of alveoli. It helps maintain pressure in smaller alveoli so that they are more equal to larger ones, allows equal aeration. Usually, the bigger alveoli would get bigger + smaller alveoli would get smaller

Answer 67

- Amniotic fluid squeezed out of lungs or absorbed into circulation - Adrenaline = increased surfactant release - Entry of O2 into lungs causes pulmonary circulation pressure to decrease as it vasodilates pulmonary arteries, increasing flow. This also prevents shunting - foramen ovale closes, ductus arteriosus constricted

Answer 68

- Fluid lining alveoli - Layer of epithelial cells (type I pneumocytes) - Basement membrane of ^ cells - Interstitial space between alveoli epithelium and capillary endothelial cells - Basement membrane of capillary endothelium - Capillary endothelial cells - Red blood cells

Answer 69

Reduced affinity.

Answer 70

- Hypoxic pulmonary constriction = decrease in ventilation within group of alveoli leads to decrease of PaO2. Vasoconstriction diverts blood away from poorly ventilated area - Local bronchoconstriction = if there is a local decrease in blood flow within a lung region, there is less systemic CO2 in area. This results in bronchoconstriction which diverts airflow away to areas of lung with better perfusion

Answer 71

IgG, IgA, IgM, IgE, IgD. Remember GAMED

Answer 72

Secrete surfactant to reduce surface tension

Answer 73

Respiratory bronchioles, alveolar ducts, alveolar sacs

Answer 74

C2, 3 and 4.

Answer 75

Phrenic nerve. 'C 3, 4 and 5 keep the diaphragm alive'. Passing through, IVC = T8, oesophagus = T10 + aorta = T12

Answer 76

Common carotid artery, internal jugular vein + vagus nerve

Answer 77

- Minute volume = 5L/min - Air into lungs via negative intra-alveolar pressure - Transpulmonary pressure = difference in pressure betweeen inside + outside of lung (alveolar pressure - intrapleural pressure) - Alveolar pressure = air pressure in pulmonary alveoli - Intrapleural pressure = pressure in pleural space

Answer 78

- Compliance = change in lung volume caused by given change in transpulmonary pressure. Greater lung compliance = more readily the lungs expand. Affected by stretchability of elastic lung tissue + surface tension of alveoli. Type II pneumocytes produce surfactant which reduces surface tension

Answer 79

- Ventilation = flow of air into + out of alveoli - Perfusion = flow of blood to alveolar capillaries - We want them to be matched

Answer 80

- reduced minute ventilation - increased dead space ventilation by rapid, shallow breathing or V/Q mismatching - increased CO2 production - PACO2 = K V'CO2/V'A

Answer 81

- CO, H+ (pH) and temperature

Answer 82

- Phrenic - Right main bronchus - Aorta and carotid bodies - Low O2, normal CO2 - COPD - Goblet cells - Diaphragm + external intercostals - pH, temperature and CO - Pre-Botzinger complex - Airway obstruction

Answer 83

- Innate: - First line of defence - Naturally present - Immediate response - Non-specific - Mainly neutrophils - Adaptive: - Often second line - Acquired - Specific - B + T-lymphocytes

Answer 84

- Phagocytes, e.g. neutrophils + monocytes - Lymphocytes

Answer 85

- Alveolar macrophages: - Arise from monocytes that circulate in blood - Functions are: microbial killing, cytokine production for coordination of inflammatory response, induction of apoptosis + clearance of apoptotic cells - Neutrophil: - Contains granules that can be primary or secondary - Functions are: identification of threat, activation, adhesion to threat, migration/chemotaxis, phagocytosis, bacterial killing

Answer 86

- B-lymphocytes: - Produced in bone marrow - Have receptors on surface that are a specific immobilised antibody - Plasma cell secretes many copies of that antibody - Antibodies bind to antigens + help in phagocytosis - Immunoglobulins: - Produced + released by B-lymphocytes - 5 types: IgG, IgA, IgM, IgE, IgD - T-lymphocytes: - Produced in bone marrow + mature in thymus gland - Involved in cell-mediated immunity through secretion of cytokines

Answer 87

Diseases in which immune responses to antigens cause inflammation + damage to the body itself

Answer 88

- Type 1: - Allergic - IgE - Causes an allergic response, e.g. hayfever, acute anaphylaxis - Type 2: - Cytotoxic - IgG/IgM - Attacks body's own cells, e.g. autoimmune diseae, Goodpasture's - Type 3: - Immune complexes - IgG - Immune complexes deposited causing local inflammation, e.g. Farmer's lung - Type 4: - Delayed, T-cell mediated - T-cells - Granulation tissues delay the response, e.g. TB, contact dermatitis

Answer 89

- Cystic fibrosis - Due to defect on long arm of chromosome 7 coding for CTFR protein (transport protein on membrane of epithelial cells - abnormal protein leads to dysregulated epithelial fluid transport) - Diagnosed through heel prick test at birth. Raised skin salt is also a sign - Symptoms include persistent cough with thick mucus, wheezing + shortness of breath, frequent chest infections, bowel disturbances, weight loss - Main complications are pneomothorax, bronchiectasis + DIOS - Patients can be given antibiotics. Given high calorie diet, segregated in hospital + monitored min. every 3 months. Can be given drugs, e.g. salbutamol nebuliser (bronchodilator). Small-molecule agents can be given for certain mutations to facilitate defective CTFR processing or function, e.g. G551D (affects 6% - there are \>1600 possible mutations)

Answer 90

- 21 kPa at sea level - PiO2 = Patm x FiO2 = 100 x 0.21 = 21kPa

Answer 91

- PAO2 = PiO2 - PaCO2/R - R = respiratory quotient = usually 0.8 but affected by diet. Calculated by CO2/O2

Answer 92

- PaO2 = 10.5 - 13.5 kPa - PaCO2 = 4.5 - 6.0 kPa - pH = 7.36 - 7.44

Answer 93

- PiO2 falls with increasing altitude - FiO2 remains constant at approximately 0.21 - PiO2 = Patm x FiO2 = 62 x 0.21 = 13kPa - PAO2 = PiO2 - PaCO2/R = 13 - 4/0.8 = 8kPa approximately

Answer 94

- Hyperventilation - Decreased PaCO2 - Alkalosis initially, until renal bicarbonate can compensate - There is an increased rate of respiration due to low O2 in surrounding atmosphere, this can lead to respiratory alkalosis as the CO2 gets breathed off

Answer 95

- 10m = 1atm, 100m = 10atm - The increase in gas density is proportional to depth below sea level

Answer 96

At a constant temperature the absolute pressure of a fixed mass of gas is inversely proportional to its volume. P1V1 = P2V2

Answer 97

1.0 x 8.9 = 16 (add one to account for sea level) x V2 V2 = 8.9/16 = 0.556 litres

Answer 98

- Total pressure exerted by a mix of gases is equal to the sum of pressures that would be exerted by each of the gases if it alone were present and occupied the total volume - Sea level: partial pressure N2 = 0.78atm, partial pressure O2 = 0.209atm

Answer 99

Injury resulting from volume changes to enclosed gas spaces - Descent = sinus, ear, tooth cavity pain - Ascent = causes increased gas volume to force expiration

Answer 100

The amount of gas dissolved in a liquid is proportional to the partial pressure of the gas above the liquid

Answer 101

Pollens, infectious agents, fungi, pets, animals, air pollution

Answer 102

Flour, car spray paints, resins, cleaning agents, laboratory animal workers, wood dusts

Answer 103

- FVC: \>80% than predicted value = normal. Low value indicates airways restriction - FEV1/FVC ratio of \<70% = airways obstruction - FEV1: \>80% than predicted value = normal

Answer 104

- PaO2 = normal - PaCO2 = low - pH = normal or reduced - HCO3 = normal

Answer 105

A (opposite from systemic)

Answer 106

An antigen is a molecule capable of inducing a specific immune response on the part of the host organism

Answer 107

- Ability to mount specific responses to a huge range of antigens - Avoids reacting to 'self' antigens - Development of immunological memory, enables more rapid + effective second response. T + B cells express different unique antigen receptors, variable region determines receptor specificity

Answer 108

- Much diversity is generated in early development via DNA rearrangements (VDJ recombination). Recombination isn't precise (nucleotides inserted or deleted), greatly increasing diversity

Answer 109

- Central tolerance = in thymus or bone marrow, lymphocytes that react with self-antigens are deleted or develop into suppressor 'Tregs' - Peripheral tolerance = in lymph nodes, autoreactive clones escaping central tolerance are deleted or suppressed by Tregs

Answer 110

Following activation, small number of high affinity B + T cells differentiate into memory cells - Allow rapid immunological response on subsequent exposure

Answer 111

- Activates cytotoxic T cells, kill pathogen-infected cells - Activates T helper cells that provide help to other immune cells, some T helper cells interact with B cells. Activated B cells proliferate, become plasma cells + make antibody (IgG, IgA, IgM, IgE, IgD). IgM produced at beginning of infection, IgG targets specific epitomes, IgE is allergic response + response to parasites

Answer 112

- Injection of dead or attenuated pathogens, harnesses immunological memory to enhance adaptive immune responses to pathogens

Answer 113

- Yes: - Failure of antibody production leads to recurrent bacterial infections - Failure of T cell function leads to 'opportunistic' infections, e.g. fungi, viruses - Failure of tolerance leads to autoimmune diseases - Failure to eliminate pathogens leads to chronic inflammation

Answer 114

- Initiating cause persists - Cellular response is innapropriate

Answer 115

B. - Motor - all the muscles which move the vocal cords (abductors, adductors or tensors) are supplied by the recurrent laryngeal nerve except the cricothyroid muscle, which is supplied by the superior laryngeal nerve = both of these are branches of the vagus nerve. - Sensory - above the vocal cords, larynx is suppied by internal laryngeal nerve, a branch of superior laryngeal nerve + below the vocal cords by recurrent laryngeal nerve

Answer 116

C. * Trachea too large * Terminal bronchiole and alveoli too small * Bronchus just right. Preferentially goes down right main bronchus due to the angle it comes off trachea.

Answer 117

A. Stimulated by increase in H+ concentration in ECF from CO2 diffusing across BBB and dissociating: H+ + HCO3- -=- CO2 + H2O

Answer 118

D. • Type 1 respiratory failure is defined as a low level of oxygen in the blood (hypoxaemia) without an increased level of carbon dioxide in the blood (hypercapnia), and indeed the PaCO2 may be normal or low. • This type of respiratory failure is caused by conditions that affect oxygenation such as: Low ambient oxygen (e.g. at high altitude) Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism) Alveolar hypoventilation due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease (this form can also cause type 2 respiratory failure if severe) Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia) Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right to left shunt).

Answer 119

B. • Type 2 • Hypoxemia (PaO2 \<8kPa) with hypercapnia (PaCO2 \>6.0kPa). • Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the build-up of carbon dioxide levels (PaCO2) that has been generated by the body but cannot be eliminated. The underlying causes include: Increased airways resistance - chronic obstructive pulmonary disease Reduced breathing effort (drug effects, brain stem lesion, extreme obesity) A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis) Neuromuscular problems

Answer 120

A. * Adrenaline causes bronchodilation, by binding to B 2 -receptors in the smooth muscle of the bronchioles and causing their relaxation. * All the other factors are associated with causing brochoconstriction