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Respiratory Block > Week #9 > Flashcards

Week #9 Flashcards

1
Q

What are some common microbiota of the respiratory tract? more than 50%

A
  • Viridans Streptococci, Neisseria spp, Corynebacterium spp, gram negative anaerobes, H.influenza, C. albicans, S. pneumoniae (15%-85%)
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2
Q

What is the most common type of bacteria living in the upper respiratory tract?

A
  • Gram negative anaerobes
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3
Q

AIDS defining illness

A
  • AIDS defining illness
  • an example is pneumocystis jiroveci
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4
Q

What are some of the causes of the common cold?

A
  • Rhinovirus, parainfluenza virus, RSV, enterovirus, coronavirus, human metapneumovirus (HMPV)
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5
Q

What are some of the common causes of pharyngitis/tonsilitis (with nasal involvement)

A
  • adenovirus, enterovirus, parainfluenza, influenza
  • (with nasal involvement is less likely to be a bacterium)
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6
Q

What are some of the causes of pharyngitis/tonsilitis (without nasal involvement)

A
  • adenovirus, enterovirus, reovirus, influenza, Strept. pyogenes, Strept groups C and G
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7
Q

Pharyngitis and tonsilitis with an associated rash is more likely to be viral or bacterial?

A
  • more likely to be a bacterial infection
  • but sometimes Group A strept infections don’t get a rash
  • A caveat is that sometimes we can get a rash when we treat amoxycillin with EBV and it is some kind of reaction between them-not indicative of treating the bacterium
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8
Q

What are some of the common causes of Sinusitis?

primary and secondary?

A
  • Common colds can spread through the tubes from the throat to the sinuses and then oince the epithelium has been damaged byt the virus it is more susceptible to bacterial infeciton from organisms that are part of the microbiota: H. influenzae, Strept. pneumoniae
  • Primary: viral (part of common cold syndrome)
    Secondary: H. influenzae, Strept. pneumoniae
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9
Q

What are some of the causes of Otitis media?

A
  • Similar to sinutis in that primary viral infection causes oem damage to the epithelium and then this increases susceptobility to infeciton form normal microbiota: Pneumococci, H. influenzae, Moraxella catarrhalis
  • ussually primary viral infection may be asymptomatic
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10
Q

What are some of the causes of Epiglottis?

A
  • very rare condition nowadays
  • caused by H.influenza type B (Hib)
  • we have the Hib vaccine now
  • very serious condition
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11
Q

Image of primary viral infections leading to secondary bacterial infections

A
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12
Q

What is the Eustachian tube?

A
  • Connects the middle ear to the nasopharynx
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13
Q

Would you do a diagnosis for the followwing:

  • Common cold
  • Pharyngitis/tonsilitis
  • sinusitis
  • otitis media
  • epiglottis
  • Croup (LTB)
A
  • unnecassary
  • if possible
  • seldom necassary
  • seldom necassary
  • whenever possible
    • cannot touch the epiglottis though
    • take X-ray to see if the epiglottis is swollen and then take blood sample as it would be a systemic infection
    • could be strange bugs etc
  • seldom necassary
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14
Q

How would we treat the folling URTI?

Note that most treatment is supportive-aspirin/pannadol etc-may become more infectious with aspirin

  • Common cold
  • Pharyngitis/tonsilitis
  • sinusitis
  • otitis media
  • epiglottiris
  • Croup (LTB)
A
  • no treatment available
  • if bacterial
    • becasue we want to prevent complications of group A strept-peri-tonsil abcess, acute rheumatic fever
    • can still use penicillin G for group A strept
  • if bacterial and severe
    • co-amoxyclav-to deal with H. influenzae or S. pneumonia
  • if <2 yo or prolonged and severe
  • essential
  • usuually none, inhaled steroids if severe
    *
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15
Q

Acute exacerbations of chronic bronchitis are commonly caused by which infectious agents?

A
  • Usually pneumococci and/or H. influenzae
    • i.e. part of the microbiota
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16
Q

What is Bronchiolitis, and what causes it?

A
  • Inflammation of the bronchioles often caused by RSV
  • long expiratory wheeze due to constriction of the airways due to inflammation
  • gas trapping
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17
Q

What are some of the causes of acute (typical) pneumonia? and what is the pattern of inflammation

A
  • Almost all cases of community acquired pneumonia is caused by streptococcus pneumoniae (pneumococci) in hospital acquired pneumonia could be more of others including H. influenzae, Staph., Klebs., Legionella, TB, Chlamydophila
  • More sudden onset, cough with sputum and blood and high fever
  • Typical pneumonia is more lobar in its site and inflammation seems to be in the alveoli
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18
Q

What are some of the causes of acute (atypical) pneumonia? and what is the pattern of inflammation? and disease course?

A
  • Most common cause is mycoplasma pneumonia (rmb doesn’t have cell wall)
  • Other causes are Chlamydia, M. catarrhalis, influenza, RSV, adenovirus, etc
  • More gradual onset, had a cough with not that much sputum and no blood.
  • diffuse and patchy pneumonia and inflammation is interstitial tissue
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19
Q

What are some of the fungal causes of pneumonia?

A
  • Histoplasma, Aspergillus, Pneumocystis
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20
Q

What are some of the causes of lung abscess

A
  • Pneumonia may have resolved but abscess is left behind
  • caused by mixed anaerobes Staph, Klebsiella
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21
Q

What is Empyema and what are some of its causes?

A
  • Empyema is pus in the pleural space
  • Staph. aureus, secondary to pneumonia
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22
Q

What are some of the must know diagnoses of Pneumonia?

and some should know pathogens

A

Must know

  • SARS, MERS
  • Influenza (H5N1 and H7N9 etc)
  • Legionella spp
    • can replicate in amoebe in cooling towers for air conditioning.
  • Bioterrorism agents-anthrax, plague etc
  • Community acquired MRSA

Should know

  • Penicillin G resistant S. pneumoniae
  • P.aurigenosa-resistant to lots of antibiotics
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23
Q

What are some clinical considerations you may make when looking at diagnosing

A
  • Community or hospital acquired
  • Underlying illness: COPD, AIDS, cystic fibrosis
  • Other risk factors:
    • contact with animal hides
      • baccilus anthracis
    • air conditioning
      • legionella
    • repotting soil
      • Legionella longbeachae
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24
Q

List some methods and mention some limitations for collecting samples to diagnose pneumoniae?

A
  • properly collected sputum
    • can be contaminated by saliva which will naturally have pneumonia causing organisms in it
    • but can then gram stain and look for PMN cells and lots of gram positive diplococci-i.e. will most likely bee streptococci pneumoniae
  • transtracheal aspirate
  • aspiration via tracheostomy, endotracheal tube
  • aspiration via bronchoscope
    • inject saline and then collect what is coughed up
  • pleural tap (if effusion)
  • lung biopsy (by needle or open)
    • not as invasive as it once was and you would do it in the case of non resolving pneumonia not responding to antibiotics
  • blood for culture and serology
    • organism is often not present in blood although if it is it would most likely be causing the pneumonia
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25
Q

When is serological diagnosis of pneumonia usefull?

A
  • Usefull in the diagnosis of hard-to-culture bacteria:
    • Mycoplasma pneumoniae
    • Legionella pneumophila
    • Chlamydophila and Chlamydia species
    • Coxiella burnetii
      • Coxciella is intracellular bacteria but doesn’t have life cycle and also causes typhus fever which is spread by arthropods
  • Look for specific Ig with rising titres
  • Antigen detection for:
    • common viruses
      • finding RSV in the upper respiratory tract is much more informative of what is going on in the lower respiratory tract. So unlike bacterial LRT taking a swab of the URT for viral infections may be more informative
    • Bordetella
    • Legionella pneumophila type 1
      • sample is actually urine
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26
Q

Treatment of Pneumonia for community acquired and non-community acquired pneumonia?

A

Community acquired pneumonia

  • Likely cause is pneumococci but we want to cover bases-Pen G/amoxycillin are to deal with pneumococci, deoxycycline/macrolide are used to deal with other causes-mycoplasma, leigonella, chlamydia are susceptible to tetracyclines and macrolides but probably resistant to penicillin

Hospital acquired

  • depends on severity and risk group
  • severity index etc and risk group
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27
Q

What is the action of glucocorticoids in asthma?

A

Glucocorticoids reduce:

  • activity, recruitment and survival of eosinophils; T lymphocytes
  • activation of mast cell cytokine production
    • although Mast cell degranulation is unchanged
  • macrophage cytokine production
    • IL-5, IL-1 and TNF-alpha are supressed as are some chemokines. IL-4 however is not supressed
  • Proliferation, cytokine and collagen production by smooth muscle and fibroblasts
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28
Q

What is the molecular mechanism of glucocorticoids?

What are the two processes of inducing the anti-inflammatory state through gene expression modification?

A
  • There are two major genomic actions but there are other non genomic actions as well.
  • The steroid engages with cytoplasmic glucocorticoid receptor which translocates into the nucleues and forms dimers which produce zinc finger transcription factors which then inter-digitate in the specific recognition sites of the promoter regions of certain genes and the consequence of the binding is typically the increase of transcription but there are also genes which are downregulated
  • So the two outcomes are either Transpression or Transactivation depending on whether the GR activates transcription or down-regulates transcription
    *
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29
Q

What is transactivation and what is the the form of the glucocorticoid which causes this modification of transcription?

What are some examples of the genes transactivatged by glucocorticoids?

A
  • Activating of anti-inflammatory genes is transactivtivation and this occurs through the GCS and the GR as a dimer (GCS/GR)2
  • Glucocorticoid-induced leucine zipper (GILZ)
  • MAPK phosphatase-1 (MKP-1)
  • Inhibitor of κBa (IκBa)
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30
Q

What is transpression and what is the the form of the glucocorticoid which causes this modification of transcription?

A
  • Transpression is where the GCS tunes down expression of some pro-inflammatory genes
  • the monomer of the GCS and the GR can interact with target proteins and then prevent signalling occuring from pro-inflammatory transcription factors through recruiting (for example) histodeacetylase-2 which can re-pack the chromatin around the promoter region which will disfavour the recruitment of the RNA polymerase and therefore prevents the trasncription of the genes IL-8, COX-2, ICAM-1, NOS2, NFκB.
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31
Q

What is the process of NFκB activation?

How does GILZ and IκBα exhert their non-inflammatory effects?

What is the process of AP-1 activation?

How does MKP-1 exhert its non-inflammatory effects?

A
  • Cytokine recepotor ligation ends up activating IκK (IκKinase) which phosphorylates the IκBα which then marks if for ubiquitination and then that undergoes proteosomal degradation which then allows NFκB to be released which then translocates into the nucleus and can then cause transcription of many pro-inflammatory genes.
  • GCS can modulate this process by upregulating IκBα and by inducing GILZ which inhibits NFκB independently of IκBα
  • JNK is a receptor for cytokines which upon phosphorylation becomes JNK-P which then recruits Jun which then becomes Jun-P which then activates AP-1 which can then activate the transcription of more pro-inflammatory genes
  • MKP-1 is able to diminish JNK phosphorylation
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32
Q

When do we use GCS to treat asthma?

A
  • If β2 agonists are needed more than 3 times a week then we need GCS
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33
Q

What are some examples of topical (inhaled) GCS?

What has the impact of the introduction of inhaled GCS for the treatment of asthma achieved on a populaiton level?

A
  • Budesonide and Fluticasone propionate is avaliable in combination with Beta-2 agonist (LABA)
  • less severe and less frequent asthma exacerbations
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34
Q

What are some example of oral GCS?

When would we use oral GCS?

A
  • Prednisolone
  • Several days: for acute exacerbations
  • Chronically: only for very severe asthma because of many side-effects
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35
Q

What are some of the side effects of inhaled GCS?

A
  • Generally well tolerated
  • Change in voice, oral thrush, decrease in serum cortisol (possibly just a measurable effect rather than one that leads to physiological outcome).
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36
Q

What are some of the side effects of oral GCS?

A
  • dose and indication limiting SE:
  • osteoporosis, diabetes, muscle wasting, hypertension, growth supression, can get withdrawal phenomenon due to the supression of the adrenal-pituitary-hypothalamic axis
  • must ween of chronic use to avoid withdrawal symptoms
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37
Q

How can oral GCS result in withdrawal symptoms?

A
  • Cortisol and synthetic GCS are able to inhibit the release of corticotrophin releasing hormone and of ACTH from the anterior pituitary gland
    so when patients are administerred GCS the adrenal gland actually undergoes atrophy due to loss of stimualtion and production of cortisol is dramatically decreased.
  • So if oral GCS are suddenly stopped the adrenal gland will not be able to repair itself that quickly and there will be a cortisol crisis
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38
Q

Methylxanthines and Phosphodiesterase Inhibitors

Provide an example and explain its function and its side effects? and provide a newer drug with fewer s.e

A
  • Theophylline
    • not entirely sure of the mechanism of action though it does have PDE inhibition activity (PDE breaks down cAMP) results in SM relaxation.
    • HDAC2 activation (prevents transcription of some genes)
    • adenosine antagonism
    • but not sure which one is the most important, if any.
  • Side effects:
    • nausea, vomiting, diarrhea, CNS stimulation, dysrythmia.
    • Also there is not much margin for error, i.e. the therapeutic doe is close to the maximal tolerated dose.
  • Roflumilast has reduced incidence and severity of SE but still some-is being used for COPD.
    • Roflumilast is a Phosphodiesterase-4 inhibitor
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39
Q

What is the chronology of asthma treatment?

assuming worsening symptoms

A
  • bronchodialtors target the bronchospasms elicitted by the leukotrienes and acetylcholine acting at M3 receptors.
  • But anti-inflammatory are needed in all but the mildest asthma to prevent the airway narrowing not dirtectly related to ASM shortening: i.e. the mucus plugs and the bronchiol wall swelling.
40
Q

Drug treatment of COPD

A
  • In COPD adding a bronchodilator may not assist in increasing FEV1
  • Even with beta agonist and muscurinic receptor antagonist
  • although this does not mean that bronchodilators do not help, there is much evidence that bronchodilators increase quality of life.
  • Perhaps FEV1 is not the best way to measure severity of the disease.
  • Perhaps we need to look at the smaller airways (less than 2mm) that contribute less the FEV1
41
Q

What is COPD?

A
  • COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients.
  • Its pulmonary component is characterized by airflow limitation that is not fully reversible.
  • The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
  • There is loss of lung parenchyma, small airways inflammation, fibrosis and thickening and pulmonary hypertension
42
Q

What is the classification system for COPD severity

A
  • GOLD1 FEV1 > 80% predicted
  • GOLD2 50% < FEV1 < 80%
  • GOLD3 30% < FEV1 < 50%
  • GOLD4 FEV1 <30%
43
Q

Lung function decline with COPD

(image)

A
44
Q

Why are GCS not as effecitive in COPD as in asthma

A
  • The activation of macrophages and neutrophils and CD8 T cells is more important in COPD than in asthma
  • The Glucocorticoids don’t work nearly as well in COPD as they do in asthma because the inflammatory cells, neutrophils and macrophages, are inherently less susceptible to GCS compared to mast cells and eosinophils.
45
Q

Pneumonia is a subset of _______

A

pneumonitis

46
Q

What are some of the pathological cnditions that can upset the alveolar capillary membrane?

A
  • pandemic H1N1 influenza can result in damage ton the parenchyma
  • Emphysema
  • pneumonitis
  • idiopathic pulmonary fibrosis
  • TB
47
Q

What are the Likely Physiological Effects of
Disrupting the A-C Membrane?

A
  1. Abnormal gas exchange
  2. Abnormal lung mechanics
  3. Pulmonary vascular complications
48
Q

How is the rate of exchange of a gas in the lung determined

A

Determined by Ficks Law

49
Q

What is the cardiac output at rest?

A
  • 5L/min
50
Q

At rest how long does a RBC spend going across the capillary in the lung-i.e. in contact with the alveoli

A
  • 0.75 seconds
  • but within the first 0.25 seconds most of the oxygenation of the blood has already occured
  • So this means that in exercise when the CO increases and perhaps the RBC only spends 0.25-0.3 seconds in the capillary there is still adequate time for diffusion
51
Q

When will the symptoms of diffusion impairment likely be noticed if moderate? and if severe?

A
  • If moderate alveolar disease there may be no symtoms of diffusion impairment at rest but upon exercise there may be less oxygenation of the blood.
  • If severe disease symptoms of diffusion impairment may be present at rest
52
Q

The gas exchange of oxygen is _____ times as effecient as it is for oxygen?

What is the consequence of this when we think about someone who is hypercapnic? i.e. what is the likely cause of the hypercapnia?

A
  • 20 times more effecient
  • Diffusion limitation for CO2 only occurs with very severe abnormalities of the A -C membrane
  • Someone with elevated PaCO2 is due to inadequate alveolar ventilation (VA)
    *
53
Q

What are the three main causes of low arterial oxygen, i.e. low PaO2

A
  • Could be due to low PiO2. E.g. at high altitude (normal A-a gradient)
  • Could be due to low ventilation (normal A-a gradient)
    • slow breathing, IV narcotics that upsets the breathing rate etc
  • Abnormal gas exchange (wide A-a gradient)
    • low V/Q
    • shunt
    • diffusion impairment
54
Q

What are some mof the posisble consequences of pathology of ther alveolar capillary membrane that result in increased WOB?

A
  • Recruitment of accessory muscles of inspiration (scalene and sternomastoid muscles)
  • Increased oxygen consumption by respiratory muscles
  • Risk of respiratory muscle fatigue, if the airway obstruction is severe
55
Q

What is the elastic work of breathing?

and if lung compliance decreases will the elastic work of breahting increase or decrease

A
  • The work needed to overcome the stiffness of the lungs to inflate them
  • Reduced compliance will result in increased elastic WOB
56
Q

what is ventilatory failure?

A
  • Failure is when PaO2 is less than 60mmHg and PaCO2 is higher than 50mmHg
57
Q

What is the resistive work of breathing

A
  • The friction of the airways as the air passes through
58
Q

Lung disease that increases the resistive work of breathing result in what spirometry and name an example of a cause of this kind of lung pathology

A
  • Result in deceased FEV1 but unchanged FVC
  • asthma is an example
59
Q

Lung disease that increases the elastic work of breathing result in what spirometry? Name an example of a cause of this kind of lung pathology

A
  • Reduced FEV1, reduced FVC
  • normal FEV1/FVC
  • An example is inflammation of lung caused by infection
  • idiopathic pulmonary fibrosis
60
Q

What two factors determine the compliance of a lung?

A
  • tissue composition
    • i.e. more tissue, more inflammatory tissue, more fibrotic tissue leads to reduced compliance
  • Surface tension in the alveoli
    • surfactant in lungs reduces the surface tension and thus increases compliance
61
Q

Does Emphysema result in increased or decreased lung compliance?

A
  • Increased lung compliance leads to hyperinflation
  • this is due to reduced lung tissue. i.e. destruction of the elastin
62
Q

What is the breathing pattern of people with lung disease resulting in reduced compliance and lung disease resultingnin airflow obstruction?

A
  • people take short shallow breaths rapidly
  • people take long deep breaths infrequently
63
Q

What is the pressure in the pulmonary circulation and what is the advantage of this level of pressure?

A
  • Pulmonary artery pressure=25/8
  • capillary pressure= 12-8 mmHg
  • this prevents fluid leaking out of the capillaries-i.e. decrease the hydrostatic pressure
64
Q

The RV and LV deliver the _____ amount of cardiac output

A

same

65
Q

A decrease in intrathoracic pressure during inspiration will _____ the compliant pulmonary vaculature and cause a consequential _____ in systollic BP upon inspiration

A
  • expand
  • decrease
66
Q

What is the anion gap?

A

Sum of the commonly measured cations and sum of the commony measure anions is called the anion gap and usually the difference is less than 15

The common ions measured are:

Na+

K+

Cl-

HCO3-

67
Q

What would be the clinical presentations of someone with pulmonary oedema due to LV failure

What would the JVP be?

would there be central cyanosis?

would there be crepitations

would the PaO2 be low or high

i.e. what would the A-a gradient be? and why?

what would be pH of the blood be and what would the cause be?

what would the anion gap be? and why?

A
  • JVP would be elavated due to increased RA pressure due to increased resistanc eof pulmoanry vasculature
  • Central cyanosis due to hypoxaemia
  • there would be crepitations due to fluid in lungs
  • The PaO2 would likely be lowered
  • A-a gradient would be widened due to low PaO2 indicating a problem with gas exchange
  • pH of the blood would be lower than normal due to a metabolic acidosis due to the increase in lactic acid build up in peripheral hypoxic muscles
  • anion gap would be greater than 15 due to the lowerred HCO3- levels which would be acting as a buffer for the increased lactic acid in the blood due to tissue hypoxia
68
Q

What is Starlings Law?

A
69
Q

Bilateral Pulmonary oedema without cardiomegaly is likely to be due to?

A
  • Hyperpermeability of the capillaries due to ARDS
  • ussually a result of some sought of inflammatory insult
  • can occur with sepsis and trauma
  • not due to increased hydrostatic pressure
  • poor gas exchange
  • low V/Q units
  • shunting which alters the ventilation
70
Q

Is there normally a leakage from capillaries into the interstitium of the lungs?

and how is this fluid removed

A
  • Yes
  • normally the fluid is removed byt the lymphatic drainage but if there is too much fluid then it can leak into the alveoli
71
Q

What are some of the mechanical changes on a lung due to pulmonary oedema?

A
  • reduced lung compliance
  • reduced lung volumes (restrictive ventilatory defect)
  • increased airway resistance
  • increased work of breathing mainly due to the reduced compliance but there may be increased resistive force due to airway compression
72
Q

What are some of the lung function changes due to pulmonary oedema?

A
  • hypoxaemia due to shunt, low V/Q units and diffusion impairment
  • Arterial blood gases
    • low PaO2, low PaCO2 (due to compensatory hyperventilation) , high pH (respiratory alkilosis)
    • But if it gets really bad then
      • increased PaCO2
        • due to decreased ventilation (respiratory acidosis) and increased lactic acid production (metabolic acidosis)
      • Type 2 respiratory failure
73
Q

Type 1 respiratory failure vs type 2 respiratory failure?

A
  • Type 1 respiratory failure is where there is normal or low CO2 levels due to hyperventilation but low O2 levels
  • Type 2 is where there is low O2 levels and high CO2 levels
74
Q

What are the 4 theoretical causes of pulmonary oedema and which ones are more clinically relevant and what can they be caused by?

A
  1. Increased capillary hydrostatic pressure
    • most common cause is LV failure
    • also mitral stenosis, fluid overload, pulmonary veno-occlusive disease
  2. Increased capillary permeability
    1. ARDS, toxins, sepsis, multiple trauma, aspiration of gastric acid
  3. (theoretical) increased osmotic pressure due to higher concentration of proteins in the blood-not clinically relevant though
  4. (theoretical) decreased lymphatic drainage
75
Q

What is an acinus?

A

Area of lung supplied by a single terminal bronchiole

76
Q

What are the cell types in the bronchi/bronchioles

A
  • respiratory epithelial cells
    • tall columnar cells
    • pseudostratified
    • ciliated
  • goblet cells
  • neuroendocrine cells
  • basal cells
77
Q

What are the cell types in the alveoli?

A
  • alveolar macrophages
  • type I pneumocytes
  • type II pneumocytes
  • Fibroblasts
  • Inflammatory cells
  • Endothelial cells
78
Q

Obstructive vs Restrictive Lung disease

Spirometry

A
  • Obstructive-primarily FEV1 is decreased may be some decrease in FVC
  • Restrictive FEV1 is normal or even increased but FVC is decreased markedly
79
Q

Asthma (definition)

A
  • increased responsiveness of airways to various stimuli leading to episodic bronchoconstriction which is at least partly reversible
80
Q

Asthma

Immediate and delayed response

A
  • Trigger causes release of inflammatory mediators which then cause an immediate response (oedema, increased mucus, and bronchospasm) and a late response (chemotaxis of eosinophils, mast cells, lymphocytes and macrophages) which leads to ongoing inflammation and eiithelial damage
81
Q

Describe how the sensitization phase of Asthma occurs?

A
  • Allergen is encountered by APC and B cell. APC differentiates T cells down Th2 pathway. Th2 cells induce isotype switching of the B cells and induce IgE pproduction from the B cell which then sensitize the Mast cell throuh FcepsilonR1 receptors
82
Q

Allergen triggered asthma: response phase, after sensitization phase. What happens?

A
  • The next time we are exposed to antigen it binds to IgE on Mast cells which leads to degranulation and then we get oedema, mucus and bronchospasm and the late phase response after that with more inflammation, macrophage, eosinophil, mast cell recruitment.
83
Q

How can asthma lead to cor pulomonale?

A
  • In severe chronic asthma
  • “Airway remodelling” – fibrosis and irreversible obstruction causes chronic hypoxia
  • chronic hypoxia leads to pulmonary vasoconstriction which leads to pulmonary hypertension which can cause cor pulmonale
84
Q

Emphysema (definition)

A
  • Abnormal, permanent enlargement of air spaces distal to the terminal bronchiole
  • From destruction of the alveolar wall without fibrosis
85
Q

What kindof Emphysema is caused by smoking and the most predominat one?

Centriacinar (centrilobular)
Panacinar (panlobular)
Distal acinar (Paraseptal)
Irregular

A

Centriacinar (centrilobular)

86
Q

How does smoke contribute to the pathology of

A
  • smoking causes imbalance between proteases and anti-proteases.
  • smoking recruits neutrophils through release of nicotine that then gomonto release elastase and ROS which further inactivates the alpha-1-antitrypsin
  • smoking inhibits alpha-1-antitrypsin
87
Q

How does emphysema cause airway obstruction?

A
  • On expiration in-elastic airways are vulnerable to collapse and this leads to decreased air exiting the lungs and hyperinflation
  • this can cause hypoxia which can then lead to cor pulmonale and pneumothorax
88
Q

Chronic Bronchitis (definition)

A
  • Persistent cough of productive sputum for at least 3 months in 2 consecutive years
89
Q

Chronic bronchitis Pathogenesis?

A
  • Pathogenesis of the larger and smaller airways whereas Emphysema is pathogenesis of the acinus
  • Chronic irritation by cigarette smoke
  • increased mucus production in large airways
  • airway inflammation, scarring and fibrosis in the smaller airways
  • Goblet cell hyperplasia
  • can get squamous cell metaplasia
90
Q

What is the Reid Index?

A
  • measures the degree of hypertrophy of the mucus secreting glands in the airway on chronic bronchitis
  • >0.4 is pathology
91
Q

What are some of the complications of chronic bronchitis?

A
  • Chronic bronchitis is often superimposed with infective exacerbations, mostly caused by microbiota of the URT that has failed to be beaten up by the stunted cilia
  • hypoxia, pulmonary hypertension and cor pulmonare
  • squamous cell metaplasia-normally no squamous epithelium in the respiratoy tract
    • normally ciliated pseudostratified columnar but change to squamous cells with smoke can lead to dysplasia and this can lead to premalignancy
92
Q

What is small airway disease?

A
  • Possibly should be called very small airway disease as chronic bronchitis is of the small airways
  • Like chronic bronchitis but confined to the terminal bronchioles
  • chronic inflammation and fibrosis
93
Q

COPD

Chronic Bronchitis or Emphysema

A
  • Pink puffer-emphysema-patients breath hard and quickly to maintain oxygen and so are not cyanosed as much
  • Blue bloaters patients tolerate hypoxia better and dont breath as quickly and become cyanosed-more likley to get cor pulmonale
94
Q

How does smoking predispose to pulmonary infection?

A
  • Inhibition of the muco-ciliary escalator
  • Increased mucus
  • Inhibition of leukocyte function
  • Direct damage to the epithelial layer
95
Q

What is Bronchiectasis?

Pathogenesis?

Causes?

Clinical course?

A

Pathogenesis

  • Severe infection of airway can lead to destruction of the airways
  • lose so much surrounding tissue that airways are dilated
  • Dilated airways are often full of ‘pus’
  • secretions begin to pool in the airway and you get more chronic infections leading to worsening bronchiectasis

Causes

  • Necrotising infections
    • Staph aureus, Influenza, Aspergillus
  • Obstruction (+ infection)
  • Cystic fibrosis
  • Cilia disorders
  • Non-infectious inflammatory conditions
    • Connective tissue diseases
    • Graft versus host disease
    • Allergic bronchopulmonary aspergillosis

Clinical course

  • severe cough productive of copious amounts of
  • foul smelling sputum
  • episodic fever
  • SOB and cyanosis
  • cor pulmonale
  • “metastatic” infection (brain)
  • amyloidosis (rare)
96
Q

What are some of the common features of restrictive lung disease?

A
  • Chronic, diffuse, non-infectious
  • Restrictive spirometry
    • decreased FVC, increased FEV1, normal FEV1/FVC
  • Inflammation and fibrosis of inter-alveolar septa
    (interstitium)
  • Diffuse reticulo-nodular and/or ground-glass patterns on CXR
97
Q

Idiopathic pulmonary fibrosis

A
  • unknown cause
  • inflammation and fibrosis at different ages scatterred across the lung in the inter-alveolar septa
  • inevitable and steady progression
  • mean survival is 3 years

Respiratory Block (4 decks)

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