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Semester 2: Cardiorespiratory Fitness > PBL Topic 2 Case 2 > Flashcards

PBL Topic 2 Case 2 Flashcards

1
Q

What is tidal volume?

A
  • Volume of air inspired or expired with each normal breath
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2
Q

What is inspiratory reserve volume?

A
  • Volume of air that can be inspired over and above the tidal volume
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3
Q

What is expiratory reserve volume?

A
  • Volume of air that can be expired after the end of normal tidal expiration
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4
Q

What is residual volume?

A
  • Volume of air remaining in the lungs after the most forceful expiration
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5
Q

How is inspiratory capacity calculated?

A
  • Tidal Volume + Inspiratory Reserve Volume
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6
Q

How is functional residual capacity calculated?

A
  • Expiratory Reserve Volume + Residual Volume
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7
Q

How is vital capacity calculated?

A
  • Inspiratory Reserve Volume + Expiratory Reserve Volume + Tidal Volume
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8
Q

How is total lung capacity calculated?

A
  • Residual Volume + Vital Capacity
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9
Q

Outline how PEFR is calculated

A
  • Blow out forcefully into the peak flow metre
  • Best of three attempts is recorded
  • Regular measurements throughout the day
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10
Q

Which condition is PEFR used to diagnose?

A
  • Asthma
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11
Q

What are the normal values of pH?

A
  • 7.35 - 7.45
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12
Q

What are the normal values of PO2?

A
  • 80 - 100 mm Hg

- 10.5 - 13.5 kPa

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13
Q

What are the normal values of PCO2?

A
  • 36 - 45 mm Hg

- 5.1 - 5.6 kPa

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14
Q

What are the normal values of oxygen saturation?

A
  • Between 95% and 100%
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15
Q

Identify two examples of obstructive airways disorders

A
  • COPD

- Asthma

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16
Q

Identify an example of a restrictive airway disorders

A
  • Fibrosis
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17
Q

How can spirometry be used to diagnose an obstructive disorder?

A
  • FEV1 is reduced
  • FVC is reduced to a lesser extent than FEV1
  • FEV1/FVC ratio < 0.7
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18
Q

How can spirometry be used to diagnose a restrictive disorder?

A
  • FEV1 is reduced
  • FVC is reduced approximately the same amount as FEV1
  • FEV/FVC ratio > 0.7
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19
Q

Outline Henry’s Law

A
  • Partial Pressure = [Dissolved Gas] / Solubility Coefficient
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20
Q

Explain why the partial pressure of CO2 is much less than that of O2

A
  • CO2 is much more soluble than O2
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21
Q

Why does oxygen diffuse into the blood from the alveoli?

A
  • Partial pressure of oxygen is greater in the gas phase than in the dissolved state
  • Movement of oxygen down a pressure gradient
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22
Q

Why does carbon dioxide diffuse into the alveoli from the blood?

A
  • Partial pressure of carbon dioxide is greater in the dissolved state than the gas phase
  • Movement of carbon dioxide down a pressure gradient
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23
Q

Outline five factors that affect the rate of gas diffusion

A
  • Partial pressure difference, ΔP
  • Cross sectional area, A
  • Solubility, S
  • Distance, D
  • Molecular weight, MW
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24
Q

How does alveolar air differ to atmospheric air?

A
  • Alveolar air has less oxygen than atmospheric air

- Alveolar air has more carbon dioxide than atmospheric air

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25
Q

Outline how alveolar air is replaced by atmospheric air

A
  • Only 1/7 of alveolar air replaced by atmospheric air with each breath
  • Improving stability of respiration
  • By preventing sudden changes in gas concentrations
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26
Q

Outline the layers of the respiratory membrane

A
  • Alveolar epithelium
  • Epithelial basement membrane
  • Interstitial space
  • Endothelial basement membrane
  • Capillary endothelium
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27
Q

What is the value of Va/Q when Va is zero and Q is normal

A
  • Zero
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28
Q

What is the value of Va/Q when Va is normal and Q is zero

A
  • Infinity
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29
Q

What is shunted blood and where does it typically occur?

A
  • Blood that is not oxygenated
  • Lower lung
  • Where Va/Q = 0
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30
Q

What is physiologic dead space and where does it typically occur

A
  • Alveolar air that is not perfused
  • Upper lung
  • Where Va/Q is infinity
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31
Q

Outline how Va/Q mismatch alters during exercise

A
  • Blood flow to upper lung increases
  • Reduced physiologic dead space
  • Va/Q is reduced to an optimum value
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32
Q

Outline how emphysema results in decreased effectiveness of the lungs in relation to Va/Q

A
  • Obstruction results in unventilated alveolar
  • Va/Q approaching zero
  • Resulting in serious physiologic shunt
  • Destruction of alveolar walls results in inadequate perfusion
  • Va/Q approaches infinity
  • Resulting in serious physiologic dead space
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33
Q

What percentage of oxygen transported from the lungs is carried in combination with haemoglobin?

A
  • 97%
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34
Q

What percentage of oxygen transported from the lungs is carried in the dissolved state in the plasma?

A
  • 3%
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35
Q

Explain how oxygen affinity changes in relation to PO2?

A
  • Where PO2 is high, e.g. in the lungs, oxygen binds with haemoglobin
  • Where PO2 is low, e.g. in the tissues, oxygen unbinds from haemoglobin
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36
Q

Explain how haemoglobin is responsible for stabilising PO2

A
  • Tissue requires 5ml of oxygen per 100 ml of blood
  • For this to occur, the PO2 must fall to 40 mm Hg
  • Therefore, PO2 cannot rise above 40 mm Hg or else not enough oxygen would be released
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37
Q

Identify four factors that cause the oxygen dissociation curve to shift to the right, what is the importance of this?

A
  • Increased acidity
  • Increased CO2
  • Increased temperature
  • Increase 2,3-BPG
  • Results in increased oxygen unloading due to the increased metabolic demands of the tissues
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38
Q

Rank the methods by which CO2 is transported in the blood in descending order

A
  • As HCO3- (70%)
  • As Hgb.CO2 (23%)
  • As CO2 (7%)
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39
Q

Outline how HCO3- is formed from dissolved CO2

A
  • Reacts with water

- Catalysed by carbonic anhydrase

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40
Q

Outline how Hgb.CO2 is formed from dissolved CO2, what is the significance of this bond

A
  • Reacts with amine radicals

- Loose bond allows CO2 to be easily released into the alveoli

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41
Q

What is the Bohr Effect?

A
  • Increase in CO2

- Causes oxygen to be displaced from haemoglobin

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42
Q

What is the Haldane Effect?

A
  • Binding of oxygen with haemoglobin displaces carbon dioxide
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43
Q

What is hypercapnia?

A
  • Excess CO2 in the body fluids
  • Initially corrected by pulmonary ventilation
  • But eventually depresses respiration
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44
Q

What is Type 1 Respiratory Failure?

A
  • Hypoxia

- Low PCO2

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45
Q

What is Type 2 Respiratory Failure?

A
  • Hypoxia

- Hypercapnia

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46
Q

Define Asthma

A
  • Hyper-reactivity of bronchial tree
  • With paroxysmal narrowing
  • Which may reverse spontaneously after treatment
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47
Q

What is Status Asthmaticus?

A
  • Asthma whereby symptoms persist for several days

- Leading to respiratory failure and death

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48
Q

Outline the pathogenesis of asthma

A
  • Th2 lymphocytes
  • Which facilitate IgE synthesis from IL-4
  • And eosinophil inflammation from IL-5
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49
Q

Outline the role of dendritic cells in the pathogenesis of asthma

A
  • Initial uptake of allergens from skin and mucosa

- Presentation to CD4 cells

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50
Q

Outline the role of mast cells in the pathogenesis of asthma

A
  • Exposure to antigen bridges two adjacent IgE molecules on mast cell
  • This triggers mast cell to release its mediators
  • Primary mediators include histamines, tryptase, prostaglandins and leukotrienes
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51
Q

Outline the role of eosinophils in the pathogenesis of asthma

A
  • Attracted by IL-3, IL-5, GM-CSF and ECF-A

- Release of leukotrienes, major basic protein and eosinophilic cationic protein

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52
Q

What is the effect of cysteinyl leukotrienes in asthma?

A
  • Bronchospasm
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53
Q

What is the effect of eosinophilic cationic protein in asthma?

A
  • Epithelial damage
  • Resulting in airway reactivity
  • Resulting in bronchospasm
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54
Q

How are cysteinyl leukotrienes activated?

A
  • Metabolism of arachidonic acid

- Via the lipoxygenase pathway

55
Q

How are prostaglandins activated?

A
  • Metabolism of arachidonic acid

- Via the cyclo-oxygenase pathway

56
Q

What is the role of ADAM 33?

A
  • Disintegrin and metalloproteinase

- Associated with tissue remodelling

57
Q

How is the epithelium affected in asthma?

A
  • Loss of ciliated columnar cells

- Metaplasia with an increase in mucous secreting goblet cells

58
Q

How is the basement membrane affected in asthma?

A
  • Deposition of repair collagens via myofibroblasts

- Thickened basement membrane

59
Q

How is smooth muscle affect in asthma?

A
  • Hyperplasia of helical bands of airway smooth muscle

- Hyperresponsiveness due to a change in actin-myosin cross-linking cycling

60
Q

Outline two ways in which neural reflexes contribute to the irritability of asthma

A
  • Central reflexes cause release of acetyl choline stimulates M3 receptors causing contraction
  • Local reflexes cause release of neuropeptides causing vasoconstriction
61
Q

Outline the clinical features of asthma

A
  • Wheezing and shortness of breath

- Made worse at night

62
Q

Outline the Hygiene Hypothesis

A
  • Components of bacteria, viruses and fungi
  • Stimulate toll-like receptors
  • Which direct response away from allergic Th2 towards protective Th1
63
Q

Explain why asthmatics wheeze after exercise or inhaling cold air

A
  • Release of histamines, prostaglandins and leukotrienes from mast cells
  • Drying and cooling makes the bronchi hyperosmolar
64
Q

Explain why asthmatics should avoid NSAIDs

A
  • Inhibit arachidonic acid pathway
  • Via the COX-1 pathway
  • Prevent synthesis of prostaglandins
  • Thus increasing production of leukotrienes
65
Q

Explain why asthmatics should avoid beta-blockers

A
  • Blockage of B2-adrenoreceptors

- Leads to bronchoconstriction and airflow limitation

66
Q

Identify five other precipitating factors in asthma

A
  • Occupational molecular weight compounds
  • Atmospheric pollution and irritants
  • Vapours an fumes
  • Diet
  • Emotional factors
67
Q

Outline the reversibility test for asthma

A
  • Inhalation of bronchodilator or use of corticosteroid
  • Results in at least a 15% increase in FEV1
  • Diagnosis of asthma
68
Q

Outline the exercise test for asthma

A
  • Run on a treadmill for 6 minutes at a speed that produced over 160 bpm
  • Results in at least a 15% decrease in FEV1
  • Diagnosis of asthma
69
Q

What may a chest x-ray show in asthma?

A
  • Overinflation
70
Q

Outline two examples of a short acting B2 adrenoreceptor agonist, how they are given and their duration of action

A
  • Salbutamol
  • Terbutaline
  • Inhalation, as and when
  • 3-5 hours
71
Q

Outline two examples of a long acting B2 adrenoreceptor agonist, how they are given and their duration of action

A
  • Salmeterol
  • Formoterol
  • Inhalation, regularly
  • 8-12 hours
72
Q

Outline the mechanism of action of B2 adrenoreceptor agonists

A
  • Bind to B2-adrenoreceptor
  • Adenylate Cyclase cAMP second messenger system
  • Bronchodilation
73
Q

Outline two other effects of B2 adrenoreceptor agonists

A
  • Inhibit mediator release from mast cells
  • Inhibit TNF-a release from monocytes
  • Increase mucous clearance by action of cilia
74
Q

Explain why B2 adrenoreceptors may cause tremor

A
  • Increase in muscle spindle discharge

- Coupled with an effect on the contraction kinetics of the fibres

75
Q

Explain why B2 adrenoreceptors may cause tachycardia

A
  • Vasodilation reduced venous return and thus reduces cardiac output
  • Also act as B1 agonists so increase heart rate by SA node
  • V
76
Q

Explain why B2 adrenoreceptors may cause dysrhythmias

A
  • Hypokalaemia

- Caused by an increased uptake of K+ by skeletal muscle

77
Q

Outline one example of a xanthine drug

A
  • Theophylline
78
Q

Outline the mechanism of action of xanthine drugs

A
  • Inhibition of phosphodiesterase enzymes, with resultant increase in cAMP (and thus bronchodilation)
  • Competitive antagonism of adenosine A1
  • Activates histone deacetylase, reversing resistance to the anti-inflammatory effects of corticosteroids
79
Q

Identify four adverse effects of xanthine drugs

A
  • Insomnia
  • Nervousness
  • Cardiac dysrhythmias
  • Seizures
80
Q

Identify an example of a muscarinic receptor antagonist

A
  • Ipratropium
81
Q

Outline the mechanism of action of muscarinic receptor antagonists

A
  • Inhibition of M3 receptors which cause smooth muscle contraction
82
Q

Explain why rifampicin reduces plasma concentration of theophylline

A
  • Theophylline is metabolised by P450 enzymes

- Rifampicin induces P450 enzymes

83
Q

Explain why erythromycin increases plasma concentration of theophylline

A
  • Theophylline is metabolised by P450 enzymes

- Erythromycin inhibits P450 enzymes

84
Q

How are xanthine drugs such as theophylline given?

A
  • Orally
85
Q

How are muscarinic receptor antagonists given?

A
  • Aerosol inhalation
86
Q

What is the duration of action of muscarinic receptor antagonists?

A
  • 3 -5 hours
87
Q

Identify an example of a cysteinyl leukotriene receptor antagonists

A
  • Montelucast
88
Q

Outline the mechanism of action of cysteinyl leukotriene receptor antagonists

A
  • Inhibition of CysLT1 and CystLT2 receptors
  • Prevent binding of LTC4 and LTD4
  • Inhibiting bronchospasm and mucous secretion
89
Q

Identify two adverse effects of cysteinyl leukotriene receptor antagonists

A
  • Headache

- GI disturbances

90
Q

What is the mechanism of action of Omalizumab?

A
  • Anti-inflammatory

- Anti-IgE antibody

91
Q

Outline the mechanism of action of glucocorticoids in asthma in relation to cytokines

A
  • Decreased formation of Th2 cytokines
  • Such as IL-4 that promotes production of IgE
  • And IL-5 that promotes activation of eosinophils
92
Q

Outline the mechanism of action of glucocorticoids in asthma in relation to vasodilators

A
  • Inhibit PGE2 and PGI2 by inhibiting the induction of COX-2

- Inhibit leukotrienes and PAF by inducing annexin-1

93
Q

Outline the main glucocorticoids used in asthma treatment

A
  • Beclometasone

- Or a higher potency Budesonide

94
Q

Outline the glucocorticoids used in acute exacerbations of asthma

A
  • Intravenous hydrocortisone

- Oral prednisolone

95
Q

Identify three adverse effects of glucocorticoids

A
  • Oral candidiasis
  • Sore throat
  • Croaky voice
96
Q

Outline the pathological basis of clear sputum

A
  • Excess secretion from bronchial mucous glands
97
Q

Outline the pathological basis of purulent sputum

A
  • Inflammatory exudate from respiratory tract infection
98
Q

Outline the pathological basis of haemoptysis

A
  • Ulceration of airways or damage to pulmonary vasculature
99
Q

Outline the pathological basis of cough

A
  • Physiological reflex response to mucous, exudate, tumour or foreign material
100
Q

Outline the pathological basis of wheezing on inspiration (stridor)

A
  • Narrowing of larynx, trachea or proximal bronchi (tumour)
101
Q

Outline the pathological basis of wheezing on expiration

A
  • Narrowing of distal bronchi (asthma)
102
Q

Outline the pathological basis of cyanosis

A
  • Increased non-oxygenated blood e.g. by impaired gas exchange
103
Q

Outline the pathological basis of pleuritic pain

A
  • Irritation of pleura due to inflammation, infarction or tumour
104
Q

Outline the pathological basis of transudate pleural effusion

A
  • A high protein effusion

- Seen in heart failure

105
Q

Outline the pathological basis of exudate pleural effusion

A
  • A low protein effusion

- Seen in inflammation or tumours

106
Q

Outline four pathological bases of finger clubbing

A
  • Lung carcinoma
  • Bronchiectasis
  • Pulmonary fibrosis
  • Cirrhosis
107
Q

Outline the pathological basis of weight loss

A
  • Protein catabolic state

- Induced by chronic inflammatory disease or tumour

108
Q

Outline the pathological basis of crackles on auscultation

A
  • Sudden inspirational opening of small airways resisted by fluid or fibrosis
109
Q

Outline the pathological basis of wheezes on auscultation

A
  • Generalised or localised airway narrowing
110
Q

Outline the pathological basis of pleural rub on auscultation

A
  • Pleural surface roughened by exudate
111
Q

Outline the pathological basis of dullness on percussion

A
  • Consolidation of lung by exudate

- E.g. pneumonia

112
Q

Outline the pathological basis of hyper-resonance on percussion

A
  • Increased gas content of thorax

- E.g. pneumothorax or emphysema

113
Q

What is meant by the term agonist?

A
  • A drug that binds to receptor and activates it
114
Q

What is meant by the term antagonist?

A
  • A drug that binds to a receptor and prevents an agonist binding to and activating it
115
Q

What is meant by the term affinity?

A
  • The tendency of a drug to bind to a receptor
116
Q

What is meant by the term efficacy?

A
  • The tendency of a drug to activate a receptor once bound
117
Q

What is meant by the term partial agonist?

A
  • A drug with partial efficacy

- (Such that even 100% of receptors are occupied the response is sub-maximal)

118
Q

What is meant by the term inverse agonist

A
  • A drug that binds to a receptor and causes negative efficacy
119
Q

How does efficacy differ in agonists, antagonists and inverse agonists

A
  • Agonist: Positive
  • Antagonist: Neutral
  • Inverse Agonist: Negative
120
Q

What is the difference between Emax and EC50/ED50

A
  • Emax is the maximal response a drug can produce

- EC50/ED50 is the concentration/dose needed to produce 50% of the maximal response

121
Q

Explain why physiological response is not directly proportional to receptor occupancy by an agonist

A
  • Enzyme degradation or rapid uptake by cells
122
Q

How does a competitive antagonism differ to other types of antagonism?

A
  • Effects are surmountable

- Meaning they can be overcome by increasing concentration of agonist

123
Q

Identify three other types of antagonists

A
  • Chemical antagonism (two substances combine in solution, effect of drug lost)
  • Pharmacokinetic antagonism (antagonist reduces absorption, metabolism or excretion of drug )
  • Physiological antagonism (two agents produce opposing physiological effects).
124
Q

According to Ley’s Model of compliance, what factors influence compliance?

A
  • Understanding
  • Memory
  • Satisfaction
125
Q

According to Ley, how can clinicians improve compliance via oral information?

A
  • Stress the importance of compliance
  • Simplify information
  • Use repetition
  • Follow up consultation with additional interviews
  • Primary effect (patients remember first thing they are told)
126
Q

What is psychosomatic illness?

A
  • Physical symptoms are produced by actions of the unconscious mind
127
Q

Identify the two forms of psychosomatic illness

A
  • No lesion of any kind and symptoms are literally psychogenic
  • Organic lesion exists though patient response is exaggerated
128
Q

Explain why general practice has a key role in management of psychosomatic illness?

A
  • At least 20% to 30% of primary care patients have medically unexplained symptoms
129
Q

What should medical care of medically unexplained symptoms include?

A
  • Improvements in communication, diagnosis and specific treatment strategies
130
Q

Identify how medically unexplained symptoms can be treated, and the limitations of this treatment

A
  • Cognitive Behavioural Therapy

- Lack of availability

131
Q

What is meant by the term compression?

A
  • Patients overestimate low risks and underestimate high risks
132
Q

What is mean by the term miscalibration?

A
  • Patients overestimate the accuracy of their own knowledge
133
Q

What is meant by the term availability?

A
  • Patients overestimate notorious risks
134
Q

What is meant by the term optimism?

A
  • Patients underestimate their susceptibility

Semester 2: Cardiorespiratory Fitness (18 decks)

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