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Phase 1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the function of the nose?

A

Filtering, defence function (cilia waft inhaled particulates from anterior naries backwards to be swallowed), temperature of inspired air

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2
Q

The anterior nares open into the vestibules. What do they contain?

A

Vestibules have turbinates. These double the SA of the nose

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3
Q

What are the spaces inbetween the turbinates called?

A

Meatus (superior, middle, inferior)

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4
Q

What are the paranasal sinuses?

A

Pneumatised areas of the:

  • frontal
  • maxillary
  • ethmoid
  • sphenoid bones

They are arranged in pairs

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5
Q

Where are the frontal sinuses found? What is their innervation?

A

Within frontal bone, midline septum. Innervated by ophthalmic division of V nerve

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6
Q

Where are the maxillary sinuses found? What is their shape?

A

Located within the body of the maxilla. Pyramidal shape

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7
Q

Where are the ethmoid sinuses found? What is their innervation?

A

Between the eyes, semilunar hiatus of the middle meatus. Ophthalmic + maxillary V nerve

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8
Q

Where are the sphenoid sinuses found? What is their innervation?

A

Medial to cavernous sinus, inferior to optic canal, dura + pituitary gland. Ophthalmic V

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9
Q

What is the pharynx? What is it split into?

A
  • Fibromuscular tube lined with epithelium. Base of skull to C6.
  • Nasopharynx, oropharynx + laryngopharynx
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10
Q

What is the function of the larynx? What is it made up of?

A

Has a valvular function. Prevents liquids + food from entering the lung. Has a rigid structure, 9 cartilages + multiple muscles. Elastic = epiglottis. Hyaline = thyroid, cricoid, arytenoid

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11
Q

What are the single and double laryngeal cartilages?

A

Single:

  • epiglottis
  • thyroid
  • cricoid

Double:

  • cuneiform
  • corniculate
  • arytenoid

Learn diagram

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12
Q

What is the laryngeal innervation? What does the main nerve split in to?

A

The vagus (X). This splits into the superior laryngeal nerve + recurrent laryngeal nerve

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13
Q

What does the superior laryngeal nerve supply? What does it divide into?

A

Inferior ganglion + lateral pharyngeal wall. Divides into internal (sensation) + external (cricothyroid muscle)

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14
Q

What does the recurrent laryngeal nerve supply? Are the left and right the same?

A

Supplies all muscles except cricothyroid (where pierced if need to get into airway). Right and left laryngeal nerve are different - left is longer than right as it crosses under arch of aorta at the ligamentum arteriosum

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15
Q

What is the general structure of the lower respiratory tract?

A

Trachea - main bronchi - lobar bronchi - segmental branches - terminal bronchiole - respiratory bronchiole - alveolar ducts + alveoli

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16
Q

Where is the trachea found? What features does it have? Is it conducting or respiratory airway?

A
  • From larynx (C6) to carina (T5)
  • Semicircular cartilaginous rings
  • Pseudostratified ciliated columnar epithelia with interspersed goblet cells
  • Conducting
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17
Q

Which bronchus is more vertical? What do these bronchi split into? Are these conducting airway or respiratory airway?

A
  • Right main bronchus is more vertical than the left - left accommodates aortic arch underneath
  • Trachea split to form these at carina
  • RMB further divides into lobar bronchi to form 3 lobes (lower, middle + upper)
  • LMB divides into lobar bronchi to form 2 lobes (upper lingular + lower)
  • Segmental bronchi arise from these lobar divisions
  • All conducting airway
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18
Q

What are the two bronchioles? Are these conducting or respiratory airway?

A
  • Terminal (conducting)
  • Respiratory = highest restriction to airflow (respiratory)
  • Conducting = no gas exchange
  • Respiratory = gas exchange
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19
Q

What do alveoli contain?

A
  • Type I (gas exchange) + II (surfactant) pneumocytes
  • Adjacent alveoli connected through pores of Kohn - allows movement of alveolar macrophages
  • Fused basement membrane with endothelia of capillaries - 1um thick

This is all respiratory. In total, there are 24 divisions from trachea to alveoli

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20
Q

What are the two types of pulmonary plurae? Where do they originate from?

A
  • Visceral - on lung surface, autonomic innervation
  • Parietal - on thoracic wall against lungs, pain sensation
  • Mesodermal origin, single layer cells
  • Continuous with each other at root of lung
  • Intrapleural fluid fills space, lubricating surfaces
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21
Q

What is the innervation of the lungs?

A
  • Sympathetic = bronchodilation (T2-4 symp. trunk ganglia)
  • Parasympathetic = bronchoconstriction (vagus)
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22
Q

What are the 7 layers of gas exchange?

A
  • Fluid lining alveolus
  • Layer of epithelial cells - Type I pneomocytes
  • Basement membrane of type I cells
  • Interstitial space
  • Basement membrane
  • Endothelia
  • Erythrocyte
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23
Q

What are the muscles of inspiration?

A
  • Diaphragm mainly, 70% of volume change (phrenic C3-5 innervation)
  • External intercostals - lift ribs 2-12, widen thoracic cavity
  • Scalenes, pectoralis major, sternocleidomastoids
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24
Q

What are the muscles of active expiration?

A
  • Passive during quiet breathing
  • Internal intercostals = depresses ribs 1-11
  • Rectus abdominis = depresses lower ribs, compresses abdominal organs + diaphragm
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25
Q

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

A
  • 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
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26
Q

What is physiological deadspace? What is it split into?

A
  • 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
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27
Q

What happens in gas exchange? What is hypoxia? How is this overcome?

A
  • 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
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28
Q

What do these abbreviations mean:

  • PaO2/CO2
  • PAO2/CO2
  • PiO2
  • V’A
  • V’CO2
A
  • Arterial O2/CO2
  • Alveolar O2/CO2
  • Pressure of inspired O2
  • Alveolar ventilation
  • CO2 production
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29
Q

What is the equation for CO2 elimination? What are the three ways in which CO2 is carried? What are the physiological causes of high CO2?

A
  • 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
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30
Q

What is the alveolar gas equation? What are the causes of low PaO2?

A
  • 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
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31
Q

What is acid base control? What carbonic acid equilibrium?

A
  • 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
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32
Q

What is the Henderson-Hasselbach equation? What are the four main acid base disorders?

A
  • 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
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33
Q

What is the innate immune response?

A

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

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34
Q

How is inflammation triggered?

A

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

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35
Q

Why is inflammation described as a ‘double edged sword’?

A

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

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36
Q

How do we recognise pathogens we have never seen before?

A

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

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37
Q

What are some specialist macrophages? What is their role in the innate immune response?

A

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

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38
Q

What are neutrophils? What is their role in the innate immune response?

A
  • 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)
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39
Q

Is the airway smooth muscle regulated?

A

Yes, it can contract + relax to regulate airway diameter

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40
Q

How are the airway smooth muscles regulated?

A
  • Regulated by autonomic nervous system (contractile signals cause increase in intracellular calcium in smooth muscle, which activated actin-myosin contraction)
  • Regulated by inflammation
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41
Q

Where does the autonomic nervous system convert all the outputs from the central nervous system to? What are the two nerves?

A
  • 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
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42
Q

What is the dominant neurological bronchoconstrictor response mediated by? What happens if there is too much bronchoconstriction?

A
  • 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
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43
Q

What does the sympathetic nervous system do to airway smooth muscle?

A
  • Nerve fibres release noradrenaline which activates adrenergic receptors on airway smooth muscles, causes muscle relaxation
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44
Q

What is the action of a beta-2 agonist on a beta-2 receptor? What are some adverse effects of beta-2 receptors?

A
  • 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
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45
Q

What factors govern drug deposition?

A
  • Particle size (main factor)
  • Flow rate
  • Underlying disease
  • Device
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46
Q

What is the difference between innate and adaptive immunity?

A
  • 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
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47
Q

What does respiratory epithelium do in the non-immune response?

A
  • Functions as a barrier to pathogens and contains mucosal glands - mucociliary escalator
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48
Q

Multiple molecules secreted from the epithelium play a role in host defence. Give examples of these molecules.

A
  • Antiproteinases (lysozymes)
  • Anti-fungal proteins
  • Anti-microbial proteins (a&b defensins)
  • Surfactants (A&D)
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49
Q

The host defence in the respiratory tract relies on more than epithelial cell products. What are the other lines of defence?

A

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

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50
Q

What is mucus?

A

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

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51
Q

What are coughing and sneezing?

A
  • Coughing = expulsive reflux with some voluntary control, clearance of irritants
  • Sneezing - involuntary reflex in response to nasal muscosa irritation or excess fluid in airway
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52
Q

Can airway epithelium repair itself?

A
  • 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
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53
Q

What are the definitions of the values measured in a lung function test?

A
  • 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
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54
Q

What is FEV1 and FVC? How are they used?

A
  • 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
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55
Q

What is the PEF? What is the flow-volume loop?

A
  • 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
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56
Q

Airways are defined as obstructive or restrictive using spirometry. What do these terms mean and what conditions are associated with them?

A
  • Obstruction = blockage of airways. Eventually reach FVC. Asthma, COPD (learn)
  • Restriction = can’t expand lungs, can’t reach FVC. Obesity, pulmonary fibrosis (learn)
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57
Q

What are the figures for the FEV1/FVC ratio and the FVC in airway obstruction and restriction?

A
  • Airway obstruction:
  • FEV1/FVC ratio = <70%, low FEV1 (<80%)
  • FVC = normal
  • Airway restriction:
  • FEV1/FVC ratio = <80%, low FEV1
  • FVC = <80%
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58
Q

Expiratory procedures only measure VC, not RV. What are some other ways to measure RV and TLC?

A
  • 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
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59
Q

What is DLCO? What is used to estimate this?

A

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

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60
Q

What is compliance? What determines lung compliance? What are the two types of compliance?

A
  • 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)
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61
Q

What is pontine system? Where is it found?

A
  • 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
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62
Q

What is the medullary system? Where is it found?

A
  • 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
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63
Q

What happens in inspiration and expiration?

A
  • 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
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64
Q

The DRG etc. need to be stimulated. What are the two types of chemoreceptors?

A
  • 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
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65
Q

What is the general rule for minute ventilation?

A

Proportional to PaCO2 and 1/PaO2

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66
Q

Explain the control by PO2 and control by PCO2.

A
  • 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
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67
Q

What are the three types of pulmonary stretch receptors? What do they cause?

A
  • 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
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68
Q

Airway receptors are either found in nose, nasopharynx and larynx or the pharynx. What do they do?

A
  • 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
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69
Q

What is the role of muscle proprioreceptors?

A
  • Important roles in perception of breathing effort
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70
Q

What do the terms hypoxia and hypercapnia mean?

A
  • Hypoxia = deficiency of oxygen at the tissue level
  • Hypercapnia = increase in PCO2 in the arterial blood. Hypercapnia is the main drive to breathe
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71
Q

What are the four types of hypoxia?

A
  • 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
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72
Q

Hypoxemia is the most common type of hypoxia. What are the four most common causes of this?

A
  • 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)
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73
Q

What is respiratory failure? What is type I respiratory failure?

A
  • 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
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74
Q

What is type II respiratory failure?

A
  • PaO2 = low (hypoxia)
  • PaCO2 = high (hypercapnia)
  • Caused by poor ventilation, e.g. COPD, asthma
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75
Q

What is the equation for PaO2?

A

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

76
Q

What is the relationship between PaCO2 and alveolar ventilation?

A

PaCO2 = 1/alveolar ventilation

77
Q

Why do we need to be more careful when treating patients with type II respiratory failure?

A
  • 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
78
Q

What are the two circulations?

A
  • 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
79
Q

What is Pouiseuille’s Law?

A
  • 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
80
Q

What is Ohm’s law?

A
  • 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
81
Q

What are these diseases examples of:

a) pulmonary embolism
b) pulmonary arterial hypertension
c) pulmonary ateriovenous malformation?

A

a) VQ mismatch
b) Increased PVR
c) Shunt

82
Q

What are the 4 stages of embryological lung development?

A
  • Embryonic (0-5 weeks)
  • Pseudoglandular phase (5-17 weeks)
  • Cannalicular phase (16-25 weeks)
  • Alveolar (25 weeks-term)
83
Q

What happens in the embryonic phase of lung development?

A
  • Lungs develop from respiratory diverticulum, an outbranch of foregut. By 5th week, lung buds enlarge to form left + right main bronchi
84
Q

What happens in the pseudoglandular phase of lung development?

A
  • Development of conducting airways (5-17 weeks)
85
Q

What happens in the cannalicular phase of lung development?

A

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

86
Q

What happens in the alveolar phase of lung development?

A
  • Alveoli develop. They further develop after birth, up to age 5
87
Q

In pulmonary circulation, is oxygen a vasodilator or a vasoconstrictor?

A

Vasodilator, hypoxia is a vasoconstrictor. Opposite in systemic circulation

88
Q

The respiratory system does not carry out physiological function of gas exchange until after birth. What veins, arteries and ducts are involved with foetal circulation?

A

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
89
Q

What is Laplace’s law?

A

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

90
Q

What is surfactant’s role in the alveoli?

A

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

91
Q

What happens in the first breath?

A
  • 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
92
Q

What are the layers of gas exchange?

A
  • 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
93
Q

What does a right shifted O2 dissociation curve mean?

A

Reduced affinity.

94
Q

What local homeostatic responses correct V/Q mismatch?

A
  • 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
95
Q

What are the five classes of antibodies?

A

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

96
Q

Comparison of sympathetic vs parasympathetic.

A
97
Q
  • What do Type II pneumocytes do?
A

Secrete surfactant to reduce surface tension

98
Q

Define Vital Capacity in spirometry.

A
99
Q

What structures are in the respiratory zone of airways?

A

Respiratory bronchioles, alveolar ducts, alveolar sacs

100
Q

Which of these is an example of airways restriction?

A. COPD

B. Pulmonary fibrosis

C. Asthma

D. Cystic fibrosis

A

B

101
Q
A
102
Q
A
103
Q
A
104
Q
A
105
Q
A
106
Q
A
107
Q

What do the superior and recurrent laryngeal nerves supply?

A
108
Q

What are the three borders of the anterior triangle?

A
109
Q

On which ribs are the inferior lung borders and inferior pleura found?

A
110
Q

Where is the lung hilum found?

A

C2, 3 and 4.

111
Q

What is the diaphragm innervated by?

A

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

112
Q
A
113
Q

What passes in the carotid sheath?

A

Common carotid artery, internal jugular vein + vagus nerve

114
Q
A
115
Q

What is the minute volume? Why does air enter lungs? What are the 3 types of pressure?

A
  • 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
116
Q

What is compliance?

A
  • 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
117
Q

What do ventilation and perfusion mean?

A
  • Ventilation = flow of air into + out of alveoli
  • Perfusion = flow of blood to alveolar capillaries
  • We want them to be matched
118
Q

What are the causes of high PaCO2?

A
  • reduced minute ventilation
  • increased dead space ventilation by rapid, shallow breathing or V/Q mismatching
  • increased CO2 production
  • PACO2 = K V’CO2/V’A
119
Q

What are the influences of the oxygen dissociation curve?

A
  • CO, H+ (pH) and temperature
120
Q

With bronchoconstriction and bronchodilation, which chemicals bind to which receptors?

A
121
Q
A
  • 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
122
Q

What are the differences between adaptive and innnate immunity?

A
  • Innate:
  • First line of defence
  • Naturally present
  • Immediate response
  • Non-specific
  • Mainly neutrophils
  • Adaptive:
  • Often second line
  • Acquired
  • Specific
  • B + T-lymphocytes
123
Q

What are the two cell types in the immune system?

A
  • Phagocytes, e.g. neutrophils + monocytes
  • Lymphocytes
124
Q

What are the two main innate immune mechanisms?

A
  • 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
125
Q

What are the three main adaptive immune mechanisms?

A
  • 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
126
Q

What is hypersensitivity?

A

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

127
Q

What are the four types of hypersensitivity according to the Gell and Coombs classification?

A
  • 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
128
Q

Give an example of a respiratory condition influenced by genetics.

A
  • 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)
129
Q

What is the pressure of inspired oxygen at sea level? How is this calculated?

A
  • 21 kPa at sea level
  • PiO2 = Patm x FiO2 = 100 x 0.21 = 21kPa
130
Q

What is the alveolar gas equation? What is R and how is it calculated?

A
  • PAO2 = PiO2 - PaCO2/R
  • R = respiratory quotient = usually 0.8 but affected by diet. Calculated by CO2/O2
131
Q

What are the normal blood gas ranges?

A
  • PaO2 = 10.5 - 13.5 kPa
  • PaCO2 = 4.5 - 6.0 kPa
  • pH = 7.36 - 7.44
132
Q

What happens to PiO2 and FiO2 as we increase in altitude?

A
  • 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
133
Q

In a normal response to increasing altitude, what does the hypoxia lead to?

A
  • 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
134
Q

For every 10 metres of sea water we descend, how many atm’s does this equal?

A
  • 10m = 1atm, 100m = 10atm
  • The increase in gas density is proportional to depth below sea level
135
Q

What is Boyle’s law?

A

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

136
Q

The total lung capacity of a 25 year old male diver is 8.9 litres at surface. What will this volume be at 150m of seawater during breath hold diving?

A

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

V2 = 8.9/16 = 0.556 litres

137
Q

What is Dalton’s law?

A
  • 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
138
Q

What is barotrauma? What may be injured when descending and ascending?

A

Injury resulting from volume changes to enclosed gas spaces

  • Descent = sinus, ear, tooth cavity pain
  • Ascent = causes increased gas volume to force expiration
139
Q

What is Henry’s law?

A

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

140
Q

What are the environmental influences of asthma?

A

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

141
Q

What are the occupational influences of asthma?

A

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

142
Q

How do we classify airways obstruction and restriction?

A
  • FVC: >80% than predicted value = normal. Low value indicates airways restriction
  • FEV1/FVC ratio of <70% = airways obstruction
  • FEV1: >80% than predicted value = normal
143
Q

What are the blood gases typically like in an asthmatic patient?

A
  • PaO2 = normal
  • PaCO2 = low
  • pH = normal or reduced
  • HCO3 = normal
144
Q
A

D

145
Q
A

B

146
Q
A

C

147
Q
A

E

148
Q
A

E

149
Q
A

D

150
Q
A

B

151
Q
A

D

152
Q
A

D

153
Q
A

A (opposite from systemic)

154
Q
A

A

155
Q
A

C

156
Q
A

A

157
Q
A

D

158
Q
A

D

159
Q
A

B

160
Q
A

D

161
Q
A

C

162
Q
A

A

163
Q
A

D

164
Q

What is an antigen?

A

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

165
Q

What are the properties of the adaptive immune response?

A
  • 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
166
Q

How do we get millions of T and B cells?

A
  • Much diversity is generated in early development via DNA rearrangements (VDJ recombination). Recombination isn’t precise (nucleotides inserted or deleted), greatly increasing diversity
167
Q

What is central and peripheral tolerance?

A
  • 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
168
Q

What are memory cells?

A

Following activation, small number of high affinity B + T cells differentiate into memory cells

  • Allow rapid immunological response on subsequent exposure
169
Q

What does antigen presentation cause?

A
  • 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
170
Q

What is vaccination?

A
  • Injection of dead or attenuated pathogens, harnesses immunological memory to enhance adaptive immune responses to pathogens
171
Q

Can our immune response go wrong?

A
  • 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
172
Q

What causes inflammation to be chronic?

A
  • Initiating cause persists
  • Cellular response is innapropriate
173
Q

Which nerve supplies motor function to the diaphragm?

A. Phrenic Nerve

B. Vagus Nerve

C. Lateral Thoracic Nerves

D. Accessory Nerve

E. Intercostal Nerves

A

A

174
Q

The Vagus Nerve supplies voluntary motor function to which of these structures?

A. Trachea

B. Larynx

C. Main bronchus

D. Nostril

E. Bronchiole

A

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
175
Q

If an adult inhales a peanut, where is it most likely to become lodged in their airway?

A. Trachea

B. Left main bronchus

C. Right main bronchus

D. Terminal bronchiole

E. Alveoli

A

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.
176
Q

What is the term used to describe a malignant tumour of the pleural membranes?

A. Pleuroma

B. Mesodermocarcinoma

C. Pleurocarcinoma

D. Mesotheliocarcinoma

E. Mesothelioma

A

E

177
Q

Central chemoreceptors are located in the ventral medulla and respond to:

A. CSF pH

B. CSF haemoglobin

C. CSF oxygen

D. CSF bicarbonate

E. CSF carbon dioxide

A

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

178
Q

The main peripheral chemoreceptors are located in the:

A. Pulmonary veins and left atrium

B. Carotid arteries and aortic arch

C. Skeletal muscle

D. Jugular veins and vena cava

E. Trachea and main bronchi

A

B

179
Q

Changes in which of these blood parameters stimulates carotid chemoreceptors?

A. Carbon dioxide and H+ ions

B. Carbon dioxide only

C. Oxygen, carbon dioxide and H+ ions

D. Oxygen and HCO3- ions

E. Carbon dioxide and HCO3- ions

A

C

180
Q

Type 1 Respiratory Failure is characterised by arterial blood gas picture of:

A. low pO2, normal/low pCO2

B. normal pO2, low pCO2

C. pO2, high pCO2

D. high pO2, high pCO2

E. high pO2, normal/low pCO2

A

A

181
Q

Which of these conditions would normally lead to Type 1 Respiratory Failure?

A. Pulmonary Hypertension

B. Widespread pulmonary tuberculosis

C. Severe Motor Neurone Disease

D. Pulmonary Embolism

E. Chronic Obstructive Pulmonary Disease

A

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).

182
Q

Chronic Type 2 Respiratory Failure is characterised by arterial blood gas picture of:

A. normal pO2, low pCO2, low-normal HCO3

B. low pO2, high pCO2, low HCO3

C. low pO2, high pCO2, normal-high HCO3

D. low pO2, low pCO2, low HCO3

E. low pO2, low pCO2, normal HCO3

A

C.

183
Q

Which of these conditions would normally lead to Type 2 Respiratory Failure?

A. Small Pneumothorax

B. Chronic Obstructive Pulmonary Disease

C. Pneumonia

D. Pulmonary embolism

E. Right middle lobe collapse

A

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

184
Q

Which of these factors will contribute to causing bronchodilation?

A. Adrenaline

B. Cold dry air

C. Beta-Blockers

D. Histamine release

E. Parasympathetic stimulation

A

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
185
Q

Which of these cells provides cilia for the mucociliary escalator?

A. Macrophages

B. Mast cells

C. Vascular Endothelial Cells

D. Goblet Cells

E. Columnar Epithelial Cells

A

E

186
Q
A

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