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UofG Medicine Question Bank 2020 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

What are things to evaluate in relation to the hands when doing a respiratory exam?

A

Pallor-
Flapping tremour- Carbon dioxide retention (impacts muscle contraction)
Blueing- peripheral cyanosis

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2
Q

What are things to evaluate in relation to the face when doing a respiratory exam?

A

Pallor of conjunctive- anaemia

Mucous Membrane blueing- central cyanosis

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3
Q

What are things to evaluate in relation to the neck when doing a respiratory exam?

A

Trachea- should feel central

Lymph nodes- looks for lymphatanotomy (neck masses), and palpate (patient sits up and you go behind to feel)

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4
Q

What are things to evaluate in relation to the chest when doing a respiratory exam?

A

Barrel chest- COPD, emphysema (prominent chest cavity)
Pectus excavatum/ carinatum- inward/outward sternum
Symmetry
Apex beat
Percussion- Should sound hollow
Chest expansion- place hands on chest wall with fingers meeting in middle, laying over, not on. Front and back
Tactile vocal phremitis- say 1-1-1 and listen for vibrations (pleural effusion, pneumothorax, pneumonia)

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5
Q

What are things to evaluate in relation to the auscultations when doing a respiratory exam?

A

Starting at apex of lungs, and moving side to side as you move down the chest wall.
3 on front, 4 on back, and in apex
Crackling course- noisy, sounds like crunchy leaves, found at base
Fine crackles- pulmonary fibrosis, found at base
Wheezing- all throughout chest- caused by narrowed airways (COPD, asthma)
Strider- upper airway obstruction, severe
Vocal phremitis- vibrations

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6
Q

What do you do at the end of respiratory exam?

A

Summarize and thank patient

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7
Q

What is chylothorax?

A

Chyle (lipid rich fluid) in thorax

Commonly found in paediatric oncology patients

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8
Q

What is empyema?

A

Collection of pus in pleural sac

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9
Q

What atelectasis?

A

Inability to expand

Can occur due to obstruction, i.e. chocking

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10
Q

Where does looping of the vagus nerve occur?

A

Left: Arch of aorta (giving off the left recurrent laryngeal branch)
Right: Level of right subclavian artery

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11
Q

How do you differentiate the phrenic and vagus nerves when examining the thorax?

A

Vagus travels in thoracic cavity posterior to the hilum, phrenic travels anteriorly

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12
Q

What is effusion?

A

Accumulation of fluid in a space (i.e. the pericardial cavity)

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13
Q

What physiological changes are associated with asthma?

A

Loss of normally functioning of airway epithelium, thickening of basement membrane, hypertrophy of smooth muscle layer.

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14
Q

What impact does the pathophysiology of asthma have?

A

Causes hyper-responsiveness to normal triggers of contraction (histamine and/or acetylcholine).
Abnormal contraction in response to usually benign triggers.

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15
Q

What are possible triggers for asthma?

A

Acute Inflammation: Allergy, Viral/bacterial infection, exercise
Drugs (that interfere with normal regulation of airway): beta-blockers, non-steroidal anti-inflammatory drugs
Cold air and scents

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16
Q

How are asthma symptoms managed?

A

Bronchospasm- treated with bronchorelaxation (beta 2 agonists like salbutamol)
Inflammation- treated with anti-inflammatories (corticosteroids, leukotriene receptor blockade, monoclonal antibodies)

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17
Q

What is the typical presentation of asthma?

A

Bronchospasm (causes wheeze, dyspnoea, exercise intolerance), and Inflammation (cough)

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18
Q

What limits ability to take a breathe?

A

Breathing is a single orifice system, so need for oxygen is balanced with need to eliminate waste

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19
Q

What are the 2 different types of airway narrowing, explain each briefly?

A

Dynamic- Rapid muscle contraction (due to histamine or acetylcholine), medium-secretions
Fixed (stiff airway wall)- smooth muscle bulking, thickened basement membrane

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20
Q

How do the pathophysiological changes associated with asthma impact the physiological response?

A

Increased smooth muscle: increased force of contraction
Mast cells in smooth muscle: Twitchy smooth muscle with variable airway calibre (big changes in sensitivity and activity of muscle impacting radius)
Increased basement membrane: loss of relaxation following contraction (loss of elasticity, chronic reduction in airway calibre leading to damage of airways)

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21
Q

What is diurnal variability?

A

Variability in smooth muscle contraction throughout the day.

Usually worse at night.

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22
Q

What type of inflammation is seen in physiological response of asthma, and how is it mearsured?

A

Eosinophilic inflammation

It causes increase in production of exhaled nitric oxide which can be measures (30ppb is normal).

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23
Q

What is reversible airflow and how is its measure related to asthma?

A

Asthma should always have reversible airflow obstruction.
Asthmatic patients should experience bronchodilation following use of nebulised salbutamol, whereas someone with chronic destructive lung disease would not have any dilation. Confirmatory test

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24
Q

What are the 3 phases needed for diagnosing asthma?

A

Smooth muscle only- trigger by direct mediator release (histamine) causing rare wheezy episodes
Chronic Inflammation- irritates smooth muscle, causes regular wheezy episodes
Acute inflammation- viral infection, ‘clinical exacerbations’

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25
Q

In type 2 inflammation relating to asthma, what are the associated cells, cytokines, prostanoids, and Igs?

A

Cells- lymphocytes H2, eosinophils, mast cells
Cytokines- IL-4/5
Prostanoids- PGE2, leukotriene D4
Ig- specific IgE (typically driving type 1 allergy)

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26
Q

What is a driving factor in terms of the immunological response during first exposure to a potential asthmatic trigger?

A

The cytokines involved during first exposure will determine response.
IL-4/5/33 will lead to mast cell response (immediate), whereas IL-12 & IFN would lead to reactive T cells (delayed, protective)

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27
Q

What receptor does histamine bind to and what is its effect on the airway?

A

Binds H1 receptor

Causes smooth muscle contraction

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28
Q

What receptor does Leukotriene D4 bind to and what is its effect on the airway?

A

Cyst LKTR

Smooth muscle contraction, airway wall oedema

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29
Q

What receptor does prostaglandin bind to and what is its effect on the airway?

A

PC2
Airway wall oedema
Inflammation and mucous secretions

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30
Q

What receptor does VEGF bind to and what is its effect on the airway?

A

VEGFR

Angiogenesis

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31
Q

What are mast cell mediators involved in asthma?

A

Histamine, Leukotriene D4, prostaglandin, VEGF

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32
Q

What are chemical ways of triggering Mast cells?

A

IgE
Salicylates (aspirin and other NSAIDs)
Strong scents

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33
Q

How does exercise trigger mast cells?

A

Increases ventilation
As humidification capacity is exceeded, drying of airway occurs causing osmotic rupture of mast cells
Mimicked by mannitol in bronchoconstriction test

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34
Q

What are other inflammatory stimuli (besides mast cells)?

A 
Viral infection (neutrophils/ lymphocytes)
Parasitic infection (eosinophils)
Bacterial (neutrophils)
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35
Q

What are inflammatory and non-inflammatory triggers of asthma?

A

Inflammatory: Allergy, infection, exercise

Non-inflammatory: scents, perfumes

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36
Q

What is a treatment for the smooth muscle contraction-aspect of asthma?

A

Beta 2 agonist
Beta-2 adrenergic receptor (7 trans-membrane unit) is bound and activated by agonist causing cAMP second messenger production resulting in smooth muscle relaxation

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37
Q

What is a treatment for the inflammation-aspect of asthma and what does the treatment do?

A

Corticosteroids: Reduces airway twitches and exhaled nitric oxide. Effective on eosinophils, lymphocytes, but macrophages are slightly resistant.
Anti-leukotriene receptor drugs: More selective. Direct effect on leukotriene D4 in airway. Effect on mast cells and smooth muscle. Good for exercise asthma

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38
Q

What are emerging treatments in asthma?

A

Monoclonal Abs
Anti-IgE biological therapy- Downregulation of IgE in mast cells
Biological therapies targeting TNF, IL-5, IL-13

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39
Q

What is bronchothermoplasty?

A

Involves sending probe into lung that heats airway, causing reduction in bulking of smooth muscle, causing reduction in twitching

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40
Q

How is nerve ablation related to asthma treatment?

A

Nerve ablation of branches of vagus nerve to reduce over-use, and result in decreased bulking

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41
Q

At rest, what are the partial pressures for oxygen and Co2, and amounts used?

A 
PO2= 13.3kPa, 250ml O2/min
PCO2= 5.3 kPa, 200mL CO2/min
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42
Q

When is breathing modulated?

A

During vocalization, emotional events, volitional control, reflexes (coughing), physiological changes (exercise, sleeping)

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43
Q

What role do chemo/mechanoreceptors provide in terms of breathing?

A

Chemo- detect chemical changes and feedback to brain on blood PO2, CO2 and pH
Mechano- feedback on mechanical status of lungs, chest wall, and airways

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44
Q

Where in the brain does breathing regulation occur?

A

Brainstem

Different neuronal groups control different aspects of breathing (i.e. respiration, upper-airway control)

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45
Q

What are peripheral chemoreceptor?

A

Small, highly vascularised, found in aortic arch (use vagus nerve to send signals to brain) and bifurcation of carotid artery (use glossopharyngeal nerve).
Send signals to nucleus tractus solitarius in brainstem.

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46
Q

What do the peripheral chemoreceptors primarily respond to?

A

Decreases in PO2.

Begins around arterial PO2 of 60 mmHg, and increases drastically at PO2 of around 45 mmHg

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47
Q

What are the central chemoreceptors?

A

Clusters of neurons in brainstem (posterior to NTS) that are activated by increases in PCO2 (hypercapnia) or decrease in pH

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48
Q

What is the relationship between PCO2 and ventilation?

A

Small changes in PCO2 have large, and immediate change to ventilation (more CO2= more acidic blood -> increased ventilation).
Large role in moment-to-moment breathing

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49
Q

What are mechanoreceptors and what do they sense?

A

Sensory receptors detecting changes in pressure, movement, and touch.
In resp. system, will detect movement of lungs and chest walls.

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50
Q

What nerve do the mechanoreceptors of the respiratory system utilize and where does this nerve go?

A

Send signals via vagus nerve to Nucleus Tractus Solitarius in dorsal brainstem.

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51
Q

What are mechanoreceptors important for?

A

Adapting and adjusting breathing

Integrating with other movements, i.e. posture

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52
Q

Where are some respiratory mechanoreceptors found, what is their stimulus, and what is their reflex?

A

Airway smooth muscle -> inflation/distension of airways -> termination of inspiration
Airway epithelium -> rapid lung inflation/deflation, or oedema -> sigh, shortened expiration

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53
Q

What is the centre in brain receiving mechano-chemoreceptor signals?

A

Nucleus Tractus Solitarius on dorsum of brainstem.
Processed by respiratory neurons (apart of ventral respiratory group) that are responsible for generating rhythm of breathing.
Also receives proprioceptive

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54
Q

What are pattern generating neurons and what are the types?

A

Pneumotaxic neurons within Pontine centre of brain
They regulate the pattern (inhale, then exhale) of inhalation and exhalation associated with breathing
Inspiratory neurons fire during inspiration
Expiratory neurons active during expiration
Vasospaning neurons fire between inhalation and exhalation

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55
Q

What are the respiratory rhythm neurons?

A

Bilateral clusters of neurons with rhythm generating patterns within pontine centre
They underlie basic rhythm (speed) of breathing

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56
Q

How do rhythmic breathing signals (innervations) move from the brain to target (describe the locations/nerves involved in transmission)?

A

Brainstem neurones produce rhythmic output
Output signal sent to spinal cord
Phrenic nerve exits spinal cord at C3-5 to innervate diaphragm
Nerves exiting at thoracic levels innervate intercostals

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57
Q

What do the ventral, pontine, and dorsal respiratory groups consist of?

A 
Dorsal:
Nucleus Tractus Solitarius
Ventral:
Nucleus Ambiguos, 
Nucleus Retroambiguous, 
Prebotzinger Complex, 
Botzinger Complex
Pontine:
Pneumotaxic Centre, 
Apneuistic Centre
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58
Q

Where does volitional of breathing control come from? Describe the movement of the action potential from origin to target.

A

Diaphragma within primary motor cortex -> descends as corticospinal tract -> through medulla where it may decussate at medullary pyramids -> synapse with lower motor neurones (directly or indirectly (interneurons) at anterior horn of C3-5) -> Motor neurons project as phrenic nerve to diaphragm

59
Q

What is the Nonus Diaphragma?

A

Found in the primary motor cortex, if stimulated, can induce hiccups

60
Q

How is partial pressure determined?

A

Looks at the fraction of a gas in the air as well as the barometric pressure (multiplied against each other- when looking at things like trachea partial gas pressure, humidity needs to be accounted for (subtract ppH20))

61
Q

What separates the red blood cells from the inside of the alveolar sacs?

A

Alveolar epithelium, fused basale laminae, and endothelium (forming capillary)

62
Q

How does oxygen travel through the blood?

A

Both dissolved, and by binding to the heme groups of haemoglobin

63
Q

How does temperature impact haemoglobin saturation?

A

Large increases in temperature result in shorter plateau period, meaning slight changes in oxygen partial pressure will result in drop in saturation levels of oxygen in haemoglobin

64
Q

How does pH impact haemoglobin saturation?

A

As pH decreases, haemoglobin affinity for O2 decreases, meaning more O2 is released from the haemoglobin, and changes in saturation of haemoglobin is more dependent on O2 content (less of a plateau, steeper rise/run).
Increase in pH and lower pCO2 shifts oxygen dissociation curve to the left, meaning saturation is reached quicker, resulting in a longer plateau. This means that a bigger change in oxygen levels are needed before saturation of haemoglobin is impacted.

65
Q

What is the oxygen carrying capacity of haemoglobin and in dissolved oxygen? Include total O2 carrying capacity per litre of blood.

A 
1g Hg combines with 1.39ml of O2
Normal blood has 150g Hb/1L of blood
O2 capacity is 150 x 1.39 =208 mL O2 / 1L of blood
Dissolved O2:
3mL/L of blood 
Total:
211 mLs O2/ 1L of blood
66
Q

How much CO2 is produced every minute?

A

200mL

67
Q

How many CO2 molecules are expired by the lungs in comparison to oxygen? Include respiratory exchange ratio.

A

80 molecules CO2 expired for every 100 O2 entering

Respiratory exchange ratio = 0.8

68
Q

How is CO2 carried in blood?

A

7% dissolved in plasma
23% bound to haemoglobin
70% converted by carbonic anhydrase into bicarbonate

69
Q

How and where is CO2 converted into bicarbonate?

A

Occurs to 70% of CO2 which has diffused into RBCs
Carbonic anhydrase causes conversion of CO2 to carbonic acid, which then dissociates into H+ and bicarbonate
HCO3 then moves out of RBC in exchange for Cl- (called chloride shift)

70
Q

What is chloride shift?

A

When Chloride is moved into RBCs in exchange for bicarbonate

71
Q

How is the CO2 conversion into bicarbonate determined?

A

By concentration of the gradients.

72
Q

How are blood acidity and CO2 linked? What equation does this all tie in to?

A

pH of blood can be stabilised by bicarbonate concentrations and bicarb, CO2, and hydrogen ion concentrations are all linked via CO2-bicarbonate pathway
Henderson Hasselbach Equation.

73
Q

What is the V/Q ratio?

A

Ratio of ventilation to blood flow.
Can be defined by:
single alveolus (alveolar ventilation/capillary flow)
or
lung (total alveolar ventilation/cardiac output)

74
Q

What is the value for V/Q in a healthy individual?

A

Alveolar ventilation- 4-6L/min
Pulmonary blood flow- 5L/min
V/Q for lung = 0.8-1.2

75
Q

What happens when ventilation and perfusion are mismatched?

A

Ventilation exceeds perfusion: V/Q >1
Perfusion exceeds ventilation: V/Q<1
This mismatching results in impaired CO2 and O2 transfer

76
Q

Why is smooth muscle so important in the bronchus?

A

It determines dilation of smaller components of airway, largely impacting breathing abilities.

77
Q

How to the sym/parasympathetic nervous system impact the lungs?

A

Activation of PSN causes smooth muscle to contract, causing bronchoconstriction
Sympathetic nervous causes bronchodilation

78
Q

What alternative nerves are involved in controlling smooth muscle in the lungs and what do they do?

A

Non-adrenergic Non-cholinergic nerves (NANC)
I.e. nitric oxide, or large peptides
Excitatory NANC work with vagus nerve to cause constriction
Overall input causes normal muscle tone
Inhibitory nerve with circulating adrenaline cause dilation

79
Q

What does the ParaNS control in the lungs?

A

Increased mucous secretion in goblet cells

Bronchoconstriction

80
Q

How does T cell pathway impact asthma development?

A

Typically, T cells will go down pathway to become Th1, but in asthma-prone people, they are more likely to convert into Th2, which will release IL-4 to activate B cells and produce IgE Abs, or IL-5/13 which will activate eosinophils

81
Q

Where do corticosteroids find/bind their receptor, and what does this generally cause?

A

Corticosteroids have binding globulin
Steroid has intracellular receptor it will bind, which when bound will produce then project zinc-feet which help it to enter the nucleus and bind DNA.
This causes;
Trans-activation of anti-inflammatory’s (Annexin-1, SLP1)
Trans-repression of inflammatory mediators (cytokines, chemokines, adhesion molecules, etc)
Cis-repression- these are negative side effects, reduction in keratin, osteocalcin, POMC, CRF-1

82
Q

Do inhaled corticosteroids have big side-effects?

A

They are destroyed by first-pass metabolism in the liver, so a lot of the side-effects are not seen.
Typically in asthma, injected and oral steroid can be used too though

83
Q

What changes are seen in smooth muscle with asthma over time?

A

Hypertrophy (more common in very severe asthma, some patients may have more hyperplasia- it can vary).
This leads to hyperresponsiveness

84
Q

What phases are involved in bronchospasm?

A

Early Phase: Immediate drop in FEV1 followed by recovery. Release of cytokines follows.
Late Phase: Caused by inflammation do to released cytokines. Hours following inhalation of allergen

85
Q

What drugs are used in treating asthma?

A

Bronchodilators- for smooth muscle (B2 agonsits, anticholinergic agents, leukotriene antagonists, Xanthines)
Anti-inflammatory drugs (corticosteroids)

86
Q

What are beta 2 bronchodilators used in treating asthma?

A

B2 adrenoreceptor agonists-
Salbutamol, terbutaline (both short-acting)
Salmeterol, Formoterol (long acting, LABA)

87
Q

What are side effects of B2 adrenergic agonists?

A

Tremor is principle side effect
Tolerance may occur (but isn’t often seen)
Excess mortality

88
Q

What are anticholinergic agents used in treating asthma?

A

Ipratropium- short acting
Tiotropium- Long acting (LAMA)
Bronchodilator, Antisecretory

89
Q

What are leukotriene antagonists used for in treating asthma, what do they do, and what are possible side effects?

A 
Mentelukast, Zafirlukast
Antagonism of cysteinyl-leukotriene type 1 receptors on target cells (smooth muscle) causing:
Mild bronchodilation 
Weak anti-inflammation
May precipitate Churg-Strauss Syndrome
90
Q

What Xanthines are used in asthma treatment?

A 
Theophylline, animophyline
Bronchodilation
Oral or intravenous 
Narrow therapeutic window
Lots of side effects ((cardiac dysthymias, seizures, GI intolerance)
91
Q

What anti-inflammatory drugs are used in treating asthma?

A

Glucocorticoids
Cromoglycate/Nedocromil (largely just paediatric use)
Anti-IgE Abs

92
Q

How do glucocorticoids work to treat asthma?

A

Decrease Th2-associated cytokines

Intracellular receptors, long onset

93
Q

What is bronchiole thermoplasty and how does it work?

A

Selectively burn part of bronchus

Damage results in inability to contract

94
Q

What is COPD?

A

Irreversible airflow obstruction
Includes emphysema and chronic bronchitis
Typically caused by smoking
Often involves alveolar macrophages and epithelial cells.
CD8 cell pathway is commonly used, neutrophils are used as well

95
Q

What is treatment for COPD?

A 
Smoking cessation
Short acting beta-agonist to treat occasional bronchospasms
LABA/ICS combinations
LAMA
LAMA/LABA
LAMA/LABA/ICS combo (less common)
Oxygen in more severe cases
96
Q

What happens to Alveoli during COPD?

A

Spongy make-up becomes porous due to alveoli breakdown, causing a reduction in surface area and poorer gas exchange

97
Q

What are the steps involved in brief innervations for smoking cessations?

A 
Ask
Advise
Assess
Assist
Arrange
98
Q

What is the Herring-Breuer Reflex?

A

Stretch of the lung inhibits the drive to inspire. This prevents over-inflation.
Its stronger in children and exercising adults
This is why people typically breathe IN before holding breath

99
Q

What factors may cause variation in breathe-holding times following inspiration?

A

Variation in sensitivity of vagal nerves
Strength of the Herring Breur Reflex
Motivation

100
Q

How would a hypoxic gas mixture impact breathing if inhaled?

A

Activate peripheral chemoreceptors resulting in increases in drive to breathe and shorter breath hold times

101
Q

How would a hyperoxic/hypercapnic gas mixture impact breathing if inhaled?

A

Silences peripheral chemoreceptors (due to hyperoxic gas) and activates the central chemoreceptors (due to hypercapnic gas)- these are antagonistic effects and demonstrate sensitivity to CO2
Hold times are therefore difficult to predict.

102
Q

How do hypercapnia and hyperoxia impact each others sensitivity?

A

Hypercapnia sensitises the response to hyperoxia

Hyperoxia desensitises the response to hypercapnia

103
Q

Is a COPD associated with productive or non-productive cough, typically?

A

Non-productive, but depends

104
Q

How would asthma and COPD differ in terms of clinical testing for the disease?

A

Post bronchodilator usage should have a large response (>400ml) in asthmatic patients

105
Q

What are some examples of objective evidence supporting an asthma diagnosis?

A 
Eosinophil/IgE type responses
PEFR variability
Spirometry (obstruction that is reversible)
Bronchial challenge (airways hyper-responsiveness)
106
Q

How does smoking impact the process of diagnosis of asthma?

A

Smoking suppresses eosinophil activity, so they may have normal nitric oxide levels when being tested
Therefore, FeNO is not diagnostic in smokers

107
Q

How many cigarettes are typically show to predict development of COPD?

A

20 cigarettes a day (a pack) for 20 years (or 10 a day for 40 years, etc).
Presents in middle age

108
Q

What factors contribute to the pathogenesis of COPD?

A 
Birth/Development (parental smokers, low birth weight)
Smoking
Air pollution
Wood Burning Stoves
Occupation
Nutrition (impacts inflammation)
Socioeconomic Status
Bacterial Colonization (infection in lung tissue)
Genetics
109
Q

How does smoking contribute to COPD development?

A

Increases prevalence of free radicals, hydrogen peroxide and tar, which all contribute to free radicals in the airway
Free radicals generates oxidative stress
Oxidative stress extenuates inflammatory pathways in the cell membrane (stimulation of EGFR leading to activation of MAPK, causing increased gene expression of inflammation)
This leads to inflammation and damage to airways

110
Q

What inflammatory pathways are involved in the mechanism of COPD?

A 
Depletion of anti-oxidants in the cells and increased lipid peroxidation leads to these pathways:
Histone Acetylation
NF-kB/AP-1
Ca++
MAPK
111
Q

What leads to the destruction of lung parenchyma in relation to development of COPD?

A

Protease/antiprotease imbalance in lung.

Excess protease enzymes (neutrophil elastase), in comparison to antiprotease enzymes (alpha1 Antitrypsin)

112
Q

What are the main factors associated with emphysema, and the physiological impact they have?

A

Loss of elastic support
results in airflow obstructions, air flow trapping, hyperinflammation, mismatch of perfusion and ventilation (results in breathlessness and increased workload- maldistribution of ventilation impacting gas exchange)

113
Q

What area of the lungs are typically impacted by emphysema, and what is an exception to this?

A 
Normal patterns most commonly impact superior areas and respiratory bronchioles (cis-acinar emphysema)
Lower lobes (distal respiratory bronchioles and alveoli) being impacted indicates a likely deficiency in alpha 1-antitrypsin (pan-acinar emphysema)- more bullae formation typically seen.
114
Q

What role does alpha1-antitrypsin have in COPD development?

A

Strongest evidence for genetic involvement in COPD
Deficiency -> early COPD development as less anti-protease (a1-antitrypsin) to counteract neutrophil elastase enzyme degrading elastase components needed in lung recoil.
Homozygotes have very low levels of production
More likely to develop COPD early on
Impacts <1% of patients w COPD
Role in developing liver cirrhosis

115
Q

What is a possible treatment for severe COPD?

A

Outpatient Oxygen Therapy (O2 concentrator)

Long Term Oxygen Therapy (for hypoxic patients (<88% O2 saturation) with arterial pO2 of <7.3 kPa)

116
Q

When is Long Term Oxygen Therapy given to those with COPD?

A

When O2 saturation is <87-88% (based on O2 curve, this is the point where partial pressures become impacted)
Consider using sooner if patient has hypertension or who experience desaturation during sleep/exertion (to be used for these scenarios)
Darker skin tones can increase o2 finger saturation reading, so confirm with arterial gas reading.

117
Q

How is predicted FEV1 determined?

A

Age, sex, race, height

118
Q

Where is reversibility assessed when measuring pre-post bronchodilator levels?

A

Only used in forced expiratory volume 1, not forced vital capacity

119
Q

What would high CO2, low O2, elevated H+, and normal bicarb indicate? How can it be treated?

A

Acute respiratory acidosis which, when compensation kicks in, will result in chronic respiratory acidosis with compensation
Type 2 respiratory failure
Can be treated with intubated ventilation, although non-invasive ventilation is safer due to the high levels of inflammation involved

120
Q

How would COPD with recurrent exacerbation appear during clinical examination of pre-post bronchodilation?

A

Low FEV1 with no reversibility
Normal/low FVC
Severe air flow obstructing (seen via ratio in post-bronchodilator measures of FEV1 and FVC)
Impairment of gas transfer

121
Q

What are multiple potential factors that could cause exacerbation in COPD?

A 
Element of asthma
Bacterial colonization 
Aspergillus (mould) sensitisation 
Hypoxia
Reflux
Underlying bronchiectasis
122
Q

What factors would likely indicate bronchiectasis?

A

Mucous hypersecretion (prone to infection)
Crackles on exams
Purulent daily sputum (yellow or green sputum- high cell debris/wbc levels)

123
Q

How do lungs sound during auscultation for COPD patients?

A

Wheeze, wouldn’t expect to hear crackles

124
Q

What clinical exam observations likely indicate COPD and/or asthma?

A

Airway symptoms: cough, wheeze, variable
Breathlessness
Wheeze on auscultation
No crackles

125
Q

What symptoms likely indicate asthma?

A

Day-to-day variation
Triggers
Nocturnal symptoms

126
Q

What symptoms likely indicate emphysema?

A

Breathlessness
Low BMI
Oxygen requirement

127
Q

What symptoms likely indicate chronic bronchitis?

A

Seasonal
Daily sputum (especially in winter)
Recurrent infections

128
Q

What symptoms likely indicate bronchiectasis?

A

Daily sputum (and cough)
Crackles
Recurrent infection

129
Q

How do chronic bronchitis and bronchiectasis differ?

A

Can be difficult to discriminate
Bronchiectasis: Chronic condition, airways of lungs become abnormally widened -> build-up of excess mucus (increases vulnerability to infection)
Chronic bronchitis: Daily productive cough, lasting 3 months of the year for at least 2 years in a row. A form of COPD

130
Q

What is the definition of obstructive airways disease?

A

Ratio of FEV1 to FVC of less than 70%

Means you can get proper amounts of air into the lungs, but this is slower due to obstruction.

131
Q

What is emphysema?

A

Damage to the alveoli, over time causing porous lungs.
Form of obstructive pulmonary disease
3 types of destruction:
Centri-acinar- Respiratory epithelium more damaged, distal alveoli more well preserved
Pan-acinar- Associated with a1-antitrypsin deficiency, impacts more distal regions near alveoli
Irregular- Parenchyma scarring and damage is scattered, independent of acinar

132
Q

What is vital capacity and how is it calculated?

A

The total amount of air that can be expelled following maximal inhalation.
Inspiratory Reserve Volume + Tidal Volume + Expiratory Reserve Volume

133
Q

What is tidal volume? Include rate and volume

A

The volume we inspire and expire during restful breathing.

Normally rate of breathing is 12–16 respiratory cycles per minute, and in adults TV is approximately 0.5 L.

134
Q

What is functional residual volume and how is it calculated?

A

This is the volume of air remaining in the lungs at the end of a normal expiration.
Expiratory Reserve Volume + Residual Volume

135
Q

What is total lung capacity and how is it calculated? What is the typical amount in a healthy adult?

A

This is all the air that it is possible for the lungs to contain.
IRV + TV + ERV + RV.
About 6L

136
Q

What significance does the FEV1/FVC ratio have when determining obstructive lung disease vs restrictive lung disease?

A 
Low ratio (<80%) indicates obstructive, as forced vital capacity does not change, but the speed you can exhale in 1 second is reduced due to increased resistance.
The ratio for restrictive lung disease would not be significantly different, whereas the total lung volume would be decreased
137
Q

Can a flow loop be used to determine FEV1?

A

Nope, time isn’t measured in flow loops, only volume and rate of flow are measured

138
Q

How would a flow loop look for someone with obstructive lung disease? Compare it to restricted lung disease.

A

Expiration would be “scooped out”, but total volume would not change, whereas in restrictive lung disease, total volume would be decreased, but the rate of expiration would not change significantly.
Expiration (positive portion of the loop) is the diagnostically significant portion of the loop

139
Q

What is Amonton’s Law?

A

States that pressure exerted by a gas is directly proportional to temperature, if the volume of the gas is held constant

140
Q

What is Boyle’s Law?

A

Pressure is inversely related to volume.

As pressure increases, volume decreases

141
Q

What is Charles’s Law?

A

Volume is directly proportional to temperature.

As temperature increases, volume increases

142
Q

What are the components of the ventral respiratory group responsible for?

A

Nucleus Ambiguos- Responsible for inspiration (control uvula, soft palate, and phalanx/larynx muscles)),
Nucleus Retroambiguous- controls external intercostals and diaphragm
Prebotzinger Complex- Sets pace (pacemakers neurons)
Botzinger Complex- Controls expiratory

143
Q

What are the components of the dorsal respiratory group responsible for?

A

Nucleus Tractus Solitarius-

Receives stretch, proprioceptive, mechano receptor signals and can initiate inspiration

144
Q

What are the components of the pontine respiratory centre responsible for?

A

Pneumotaxic Centre - Fine tunes respiratory depth and rate via transitioning inspiration to expiration
Apneuistic Centre- Controls inspiration (causes apneusis - prolonged inspiration)

UofG Medicine Question Bank 2020 (42 decks)

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