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PHTY205 > Conditions > Flashcards

Conditions Flashcards

1
Q

what does the CFTR gene control?

A

controls ion transport channels of Cl- across the cell membrane

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2
Q

what happens with the mutation in the CFTR gene?

A

airway surface layer = dehydrated and cilia can no longer function properly

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3
Q

summary order of CFTR mutation:

A
  1. CFTR gene defect
  2. defective ion transport
  3. airway surface liquid depletion
  4. defective MCC
  5. mucus obstruction
  6. infection + inflammation
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4
Q

what does disease severity and progression depennd on?

A

o The gene type
o How well patients
are managed

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5
Q

what are the main respiratory changes in CF?

A
  • Submucosal gland hypertrophy
  • Increased goblet cells
  • Destruction of airway walls (bronchiectasis)
  • Cyst formation
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6
Q

how are newborns diagnosed with CF?

A

New born screening (heel prick test): if positive, then follow up sweat tests are carried out

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7
Q

symptoms of CF

A

-SOB
- recurrent lung infections
- wheeze
- cough +/- sputum

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8
Q

systems affected by CF

A
  • Respiratory
  • Endocrine
  • Digestive
  • Hepatobiliary
  • Musculo-skeletal
  • (Urinary incontinence)
  • Reproductive
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9
Q

how is the pancreas involved in CF?

A
  • insufficient secretion of enzymes
  • malabsorption of fats and some proteins
  • smelly stools + deficiencies in vitamins A, D, E & K + risk of malnourishment
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10
Q

how do you manage the pancreatic involvement in CF?

A

pancreatic replacement therapy

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11
Q

what is CF related diabetes (CFRD) due to?

A

blocked pancreatic ducts, is a very common complication in adults with CF (15-30%) & indicates disease severity

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12
Q

what is pancreatic replacement therapy?

A

aids the absorption of fats and must be taken with all meals

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13
Q

what do CF patients require in a diet?

A

high in fats & protein + supplements

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14
Q

how does CF affect the bile?

A

bile becomes thick and tenacious and the bile duct blocks leading to:
– cholestasis
– gall stones and
– eventually cirrhosis

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15
Q

what is the acute exacerbation of CF known as?

A

bronchectasis due to CF

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16
Q

bronchiectasis definition

A

the abnormal, irreversible dilation of the bronchi, where the elastic and muscular tissue is destroyed by acute/ chronic inflammation and infection

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17
Q

bronchiectasis due to CF definition

A

Mutation of the CFTR gene which alters the salt concentration in the blood (controls Cl diffusion across membrane) –> excess CL in blood –> damage to MCC (dehydrated airway surface and mucous)–> mucous plugs in airways = infection & inflam

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18
Q

pathology bronchiectasis

A
  • permanent dilation of the bronchi and bronchioles
  • loss of cilia –> squamous cells replace cilia cells
  • squamous cell metaplasia
  • mucous gland hyperplasia (mucous production)
  • can be focal/ diffuse area
  • damage to elastic and muscular tissue impairs natural drainage of bronchial secretions using Mucociliary escalator
    o secretions become chronically infected
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19
Q

bronchiectasis infection method

A
  1. initial infection
  2. inflammation in airways  cytokines, neutrophil enzymes, bacterial products
  3. impaired mucociliary clearance (because of inflam)
  4. airway mucous hypersecretion (mucous gland hyperplasia) & obstruction (due to impaired MCC)
  5. mucous plug forms in airways
  6. microbial colonisation/ infection
  7. bronchial dilation/ airway destruction
  8. inflammation in airways etc. etc.
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20
Q

bronchiectasis DUE TO CF pathogenesis

A
  • CFTR dysfunction causes dysfunctional sodium channels
  • Excessive sodium and water reabsorbed into the airways
  • Dehydration of the airway surface and mucous
  • Compresses and reduces effectiveness of cilia, impairing both MCC and cough effectiveness
  • Increased frequency chest infections
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21
Q

what does a contrast-enhanced CT show for bronchiectasis?

A

grossly dilated airways & cystic changes

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22
Q

bronchiectasis causes

A
  • congenital conditions with MC dysfunction
    e.g. primary cilial dyskinesia (PCD), CF
  • airway obstruction & then irritation & infection
  • inherited genetic disease
  • autosomal recessive pattern 1:4 change of inheriting if both parents are carriers of gene
  • thick tenacious mucous
  • COPD & Asthma
  • allergy, aspiration
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23
Q

bronchectasis causes summary

A
  • CF
  • mucous in airways that cant be cleared so it gets infected
  • foreign bodies in airways that cant be cleared so causes infection and distruction of bronchiole walls etc.
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24
Q

signs of CF

A
  • cough with excessive sputum (>30 mL/day)
    –> loose cough
    –> purulent secretion
    –> +/- haemoptysis (due to inflamed airway mucous)
    –> thick, tenacious sputum
  • reports recurrent exacerbations / infections needing antibiotics (patients with >3 exacerbations/year)
  • dyspnoea
  • fatigue
  • recurrent pulmonary infections
  • execise intolerance
  • R sided heart failure
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25
Q

symptoms of CF

A
  • chronic cough
  • thick tenacious sputum
  • recurrent pulm infections
  • recurrent eps of bronchitis, pneumonia, bronchiectasis
  • ## exercise intolerance
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26
Q

bronchiectasis due to CF chest X-Ray

A
  • Thickening of bronchial walls
  • Irregular shaped bronchioles
  • Mucous plugging
  • Widespread ‘patchy’ opacities/ mucoid impaction
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27
Q

bronchectasis due to CF ABG

A
  • Extensive disease may result in hypoxaemia
  • Raised PaCO2 = rare
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28
Q

CF bronchiectasis PFT

A

Obstructive Pattern
- FVC decreased
- FEV1 decreased
- TLC normal
- DLCO normal
- FEV1/FVC <70% predicted

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29
Q

CF bronchiectasis auscultation

A

variable
- coarse crackles on inspiration & expiration (mucous in airways)
- wheeze (narrowed airways)

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30
Q

IMPAIRMENTS DUE TO CF BRONCHIECTASIS
secretion movement impairment (MCC)

A

decreased MCC
- dehydration of the airway surface (CFTR gene mutation) = destroys cilia
- primary disruption to the airway lining (inflammation) affects MCC
- decreased MCC = mucous plugging = infection of mucous = damage to the bronchioles = bronchiectasis

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31
Q

what does destruction and dilation of airways cause?

A

‘floppy airways’ (obstruction on expiration)

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32
Q

what does chronic CF infection cause?

A

fibrosis of lung parenchyma

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33
Q

what does fibrosis of lung parenchyma disrupt?

A

O2 movement across membrane

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34
Q

IMPAIRMENTS DUE TO CF BRONCHIECTASIS
Secretion movement (cough)

A
  • airflow limitation (cant get air out during expiration) – cant get air behind cough = ineffective cough
  • thick mucous plugs in airways + ineffective cough (due to lack of O2/ floppy airways (cant get air out)) = obstruction
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35
Q

what happens to the airways in CF bronchiectasis

A

floppy and fibrosed (due to recurrent infections)

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36
Q

what does CF bronchiectasis damage?

A
  • lung parenchyma
  • lung compliance (decreases lung compliance)
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37
Q

IMPAIRMENTS DUE TO CF BRONCHIECTASIS
Gas movement (O2)

A

permanent scarring of lung parenchyma, due to chronic infection, decreases O2 movement across airway walls (also as they are fibrosed & floppy - reduced SA)

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38
Q

IMPAIRMENTS DUE TO CF BRONCHIECTASIS
Pump effectiveness (e.g. NMC, muscles, bones)

A

decreased pump effectiveness

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39
Q

IMPAIRMENTS DUE TO CF BRONCHIECTASIS
Gas movement (CO2)

A

decreased CO2 movement as floppy airways disable the air (CO2) from coming out of body on expiration

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40
Q

NON CF bronchiectasis definitoin

A

progressive condition with irreversible destruction & dilation of airways

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41
Q

pathology of non CF bronchiectasis

A
  • chronic inflammatory changes
  • damage to airway structures
  • dilation of airways
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42
Q

Non CF bronchiectasis pathogenesis

A
  • Recurrent infection/ inflammation damage bronchi and bronchioles
  • Loss of elastic and muscular tissue (due to repeated infection) = dilation of bronchi
  • Loss of cilia impairs MCC
  • Remaining bacteria remains in airways and colonise mucous
  • Dilated ‘floppy’ airways = airflow obstruction
  • Cilia dysfunction and mucous production cause this cycle to repeat causing disease progression
  • Excessive sputum production (mucous gland hyperplasia) and impairment to MCC = airflow limitation
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43
Q

non CF bronchiectasis signs & symptoms

A
  • Chronic productive cough–> sputum production
  • Copious amounts of purulent, foul-smelling, green or yellow sputum
  • Haemoptysis sometimes
  • Dyspnoea –> due to airflow limitation on expiration (O2 movement is impaired as it cant diffuse across membrane walls easily as they = inflamed, thick, swollen, mucous plugging
  • digital clubbing
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44
Q

non CF bronchiectasis auscultation

A

coarse crackles on inspiration and expiration (mucous plugging and mucous in airways)

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45
Q

non CF bronchiectasis CXR findings

A
  • Thickening of bronchial walls
  • Irregular shaped bronchioles
  • Mucous plugging
  • HRCT scan is gold standard
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46
Q

Non CF bronchiectasis ABG

A
  • extensive disease may result in hypoxemia
  • raised PaCO2 = rare
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47
Q

non CF bronchiectasis PFT

A

obstructive pattern
- decreased FVC
- TLC normal
- decreased FEV1
- DLCO normal
- FEV1/ FVC <70%

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48
Q

IMPAIRMENTS OF NON CF BRONCHIECTASIS
Secretion movement (MCC + cough)

A

decreased MCC (due to destruction of airway walls?) –> secretion movement issue –> ineffective cough

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49
Q

IMPAIRMENTS OF NON CF BRONCHIECTASIS
Gas movement (O2)

A

destruction & dilation of airways causes ‘floppy’ airways & scarring of lung parenchyma
–> disrupts O2 movement across membrane (reduced SA + destruction of airway walls)

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50
Q

COPD
Chronic Bronchitis definition

A

expectoration of COPD on most days for at least 3 months in the year for at least 2 consecutive years

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51
Q

chronic bronchitis pathology

A
  • mucous gland hypertrophy–> increased mucous production & decreased clearance
  • structure of the airways is damaged –> damage to the secretion movement of the airways e.g. mucociliary clearance
  • cilial dysfunction –> cant clear mucous from airways
  • chronic inflammation of small airways –> narrowing, cellular infiltration, airway wall oedema
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52
Q

chronic bronchitis symptoms

A
  • increased mucous production
  • increased sputum production (cough +/- sputum)
  • shortness of breath
  • abnormal pattern of breathing
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53
Q

chronic bronchitis signs

A
  • increased sputum production
  • abnormal pattern of breathing
  • hyperinflated lungs
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54
Q

chronic bronchitis auscultation

A

reduced breath sounds, coarse crackles

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55
Q

chronic bronchitis PFT

A
  • Decrease FEV1/FVC
  • decrease FEV1 %
    obstructive pattern
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56
Q

chronic bronchitis ABG

A

PaCO2 increases and PaO2 decreases, SpO2 decreases

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57
Q

why is bone disease common in CF?

A

they have low BMD

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58
Q

why do CF patients have low BMD ?

A

decreased rates of bone accretion, and increased rate of bone loss

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59
Q

how do you MAXIMISE peak bone mass in adolescents?

A
  • Regular WB exercises (plyometric – jump/hop/skip etc)
  • Strength and resistance training
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60
Q

what do adults with CF have with bones?

A

accelerated bone loss

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61
Q

how can you maintain bone mass & slow the rate of loss in adults with CF?

A
  • Exercise (WB, PA/ resistance training)
  • Diet
  • Medications
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62
Q

what are the fracture rates like in the CF population?

A

high

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63
Q

what can fractures in CF patients contribute to?

A

throacic kyphosis

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64
Q

why is screening for M/S pain (acute and chronic) a key aspect of CF care?

A

patients live longer

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65
Q

how does CF affect chest shape?

A

hyperinflated chest –> tight postural muscles & pecs

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66
Q

what movements does CF limit?

A

shoulder and neck flexion

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67
Q

what postural position does CF cause ?

A

Thoracic kyphosis

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68
Q

why are females with CF encouraged to reach optimum nutrition and lung function before pregnancy?

A

– to aid conception
– to minimise the detrimental effects pregnancy will have on these symptoms

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69
Q

potential causes of incontinence in CF:

A

– Chronic cough or paroxysms of prolonged coughing
– Demands placed on the pelvic floor during airway clearance therapy, (eg, huffing, coughing & exercise)
– Underlying structural differences

70
Q

CF Rx methods

A
  • Prevent acquisition of bacteria (prevents bronchiectasis –> chronic infection of the clogged mucous)
  • Strict infection control ( Staff and patients)
  • Isolation of inpatients
  • Pathogen specific clinics
  • Discourage socialisation (between those with CF)
    except in well ventilated large open spaces
  • Airway clearance techniques
  • *Modulator therapies
  • antibiotics
71
Q

purpose of antibiotics in CF

A

Attempt to eradicate bacteria on first presentation with aggressive therapy combinations

72
Q

different ways to insert antibiotics into blood

A

IV, inhaled or oral
* In hospital or IV at home
* IV therapy via
– Peripherally inserted central line (PICC) or
– Portacath

73
Q

how is hypertonic saline used as a Rx for CF?

A

The body tries to dilute this strong salt solution by the
release of water into the airways

74
Q

what happens to the secretions after inhaling hypertonic saline?

A

The secretions become less viscous & are therefore more
easily expectorated

75
Q

wht can hypertonic saline induce?

A

bronchospasm in clients with reactive airways (adminster with ventolin)

76
Q

how is dornase alfa (pulmozyme) administered?

A

via nebuliser in people with CF who have thick viscous secretions containing decaying inflammatory cell and bacteria

77
Q

what is pulmozyme

A

Recombinant human deoxynuclease

78
Q

how does pulmozyme work?

A

Cleaves long strands of DNA into smaller strands and
thereby “liquefies” sputum making it easier to clear

79
Q

what type of agent is mannitol?

A

Osmotic agent

80
Q

how does Mannitol help in CF?

A

Decreases viscosity of secretions

81
Q

Rx regimens in CF:

A
  • Antibiotic treatments (oral
    or intravenous): 80—95%
  • Nebulised medicines and
    pancreatic enzymes: 65—
    80%
  • Vitamin therapy, dietary
    management, exercise
    regimens and physiotherapy
    airway clearance: 40—55%
82
Q

how does a decreased MCC in CF create a secretion movement problem?

A

cilia = ineffective in clearing mucous (they are dried out due to the airway wall dehydration) = recurrent infections and further cilial damage

83
Q

how is the mucous a secretion movement factor in CF?

A

viscosity increases (thicker & stickier) which then causes the cilia to be ineffective

84
Q

how does CF affect airways?

A

recurrent infections lead to floppy airways (damaged & fibrosed)

85
Q

how does CF affect lung parenchyma?

A

recurrent infection leads to damage (fibrosis) of alveoli, interstitium, capillaries

86
Q

how does CF cause a weak/ ineffective cough?

A

obstruction on expiration = decreased EFR = decreased volition = decreased cough effectiveness

87
Q

what happens to the inspired volumes in CF?

A

decreased

88
Q

what happens to lung compliance in CF?

A

decreased

89
Q

respiratory load in CF?

A

increased

90
Q

Pneumonia definition

A

An acute inflammatory condition of the lung parenchyma

91
Q

pneumonia pathology

A

Alveolar spaces are filled partially or completely with fluid and blood cells (infectious debris & exudate)

92
Q

how can pneumonia be classified?

A
  1. site of infection
  2. source
  3. cause
93
Q

pneumonia classification by site of infection

A
  • Lobar pneumonia
  • Bronchopneumonia
94
Q

pneumonia classification by source of infection

A
  • Community acquired pneumonia (CAP)
  • Nosocomial / hospital acquired
  • Ventilated acquired pneumonia (VAP)
95
Q

pneumonia classification by cause of infection

A

aspiration pneumonia, pneumocystis carinii pneumonia (fungi)

96
Q

on the CXR, what are the telltale features of lobar pneumonia?

A
  • consolidation
  • no loss of lobe vol
  • air bronchograms
97
Q

on the CXR, what are the telltale features of bronchopneumonia?

A

patchy distribution of consolidation
- air bronchograms (air trapped in airways)

98
Q

risk factors of pneumonia

A
  • stroke
  • poor nutrition
  • smoking
  • alcoholism
  • winter
  • extremes of age
99
Q

PATHOGENESIS OF PNEUMONIA
Stage 1: hyperaemia/ congestion

A

acute inflammatory response (first 24 hours)

100
Q

PATHOGENESIS OF PNEUMONIA
Stage 2: red hepatisation (2-3 days)

A

alveoli fill with RBC, exudate, and fibrin

101
Q

PATHOGENESIS OF PNEUMONIA
Stage 3: grey hepatisation (4-8 days)

A

WBC colonise area and phagocytosis of cell debris occurs

102
Q

PATHOGENESIS OF PNEUMONIA
Stage 4: resolution (8days -weeks)

A

immune & inflammatory responses decrease, macrophages clearn up area

103
Q

what happens to Pneumonia in terms of obstructive & restrictive?

A

starts as obstructive AF limitation gas mvmt impairment due to increased distance of exchange additional inflammation leads to restrictive airflow changes

104
Q

signs/symptoms of Pneumonia

A

– Cough ± sputum/haemoptysis
– ± Chest wall (pleuritic) pain
– Changed pattern of breathing

105
Q

ausc of pneumonia

A
  • wheezing
  • decreased BS
  • fine crackles (alv opening to get more air)
106
Q

aspiration definition

A

inhalation of either oropharyngeal or gastric contents into the lower airways

107
Q

what is aspiration pneumonia

A

aspiration of bacteria from
oral and pharyngeal areas

108
Q

what can aspiration pneumonia result in?

A

– Purulent sputum
– Tissue necrosis
– Pulmonary cavities (anaerobic lung abscess)

109
Q

pneumonia CXR & ABG

A

– CXR: infiltrate/opacity
– ABG changes (reduced PaO2)

110
Q

Pneumonia constitutional symptoms (indicate acute infection)

A

– Fever
– Myalgia
– Malaise
– Tachycardia

111
Q

how does pneumonia affect secretion movement?

A

infection causes cilial dysfunction and loss (inability to move secretions), some pneumonias will have mucus

112
Q

what happens to the alveoli in pneumonia?

A

infection and its by-products fill the alveoli

113
Q

how does Pneumonia cause an O2 movement problem?

A

filling of the alveoli with exudate decreases surface area and decreases O2 diffusion across membrane

114
Q

is lung compliance increased or decreased in pneumonia?

A

decreased

115
Q

how can a decreased O2 movement affect the cough?

A
  • decrease volition
  • decrease size of breath in
  • decrease cough effort
    (cant get big breath behind it)
116
Q

how does pneumonia affect muscles?

A

inflammation of the pleura causes pain –> impacts muscle function

117
Q

medical management of pneumonia

A
  • antibiotics
  • other drugs to decrease airway inflamm
  • supportive therapies e.g. o2 therapy
  • physio management e.g. AC techs
118
Q

why do indigenous australians have a higher incidence of bronchiectasis?

A

linked to
poorer health and lack of antibiotic use

119
Q

causes of bronchiectasis

A
  1. congenital conditions with MC dysfunction
  2. immune deficiencies
  3. Airway obstruction (inhalation/tumour)
  4. Aspiration (reflux)
  5. Allergic bronchopulmonary aspergillosis (ABPA)
  6. COPD and Asthma: numbers underreported
  7. Idiopathic Bronchiectasis associated with NTM
120
Q

signs & symptoms of bronchiectasis

A
  • Cough with excessive sputum (>30ml/day)
  • Reports recurrent exacerbations
  • Dyspnoea
  • fatigue
121
Q

bronchiectasis auscultation s

A

variable e.g. coarse crackles (sputum in airways), wheeze

122
Q

bronchiectasis spirometry

A

mixed pattern

123
Q

bronchiectasis CXR/CT scan

A

HRCT scan better for diagnosis &
monitoring progression than CXR

124
Q

how does bronchiectasis affect MCC?

A

infection causes disruption to airway lining: MCC, specifically cilia
- infection causes loss of cilia

125
Q

how does a decreased MCC cause a secretion movement problem?

A

long term effects of decreased MCC = chronic infection (mucus) and damage to airway
- cant clear mucus due to loss of cilia - mucus clogs airays = infected

126
Q

what happens to the airways in bronchiectasis?

A

destruction & remodeling

127
Q

how does bronchiectasis effect cough?

A

obstruction on expiration decreased EFR

128
Q

how does bronchiectasis affect airway resistance?

A

destruction and dilation causes ‘floppy’ airways (obstruction)
- increases airway resistance

129
Q

how does chronic infection affect the parenchyma in bronchiectasis?

A

results in fibrosis of lung parenchyma

130
Q

goals of Mx of bronchiectasis

A

to optimise:
- General well-being
- Symptom control
- Quality of life (QoL)
- Reduce exacerbation frequency
- Prevent excessive decline in lung function

131
Q

stepwise Rx approach of symptomatic BE

A
  1. treat underlying cause e.g. foreign body
  2. optimise airway clearance (e.g. techniques), inhaled mucokinetics
  3. treat infection (acute and chronic)
    - oral antibiotics (10days)
    - IV antibiotics (5-14 days)
132
Q

what does a restrictive disorder do on inspiration?

A

Prevents adequate volume entering the lungs

133
Q

what happens to FVC and FEV1 with restrictive disorders?

A

decreases (ratio is normal or slightly increased)

134
Q

tidal volume wih restrictive disorders

A

decreased ( with compensatory increased RR)

135
Q

examples of disorders causing restriction

A
  • Neurological injury or disease below the brainstem
  • Weak respiratory muscles
  • Skeletal chest wall is stiff or too floppy
  • Disorders of the pleural space
  • Stiff lungs
136
Q

what do restrictive disorders generally affect?

A

the respiratory pump e.g. muscle, pleura, skeletal system, NM

137
Q

types of NM disorders that cause restriction

A
  • Transmission of signals to muscles is reduced/absent
  • Neuropathies
  • Neuromuscular junction abnormalities
  • Muscle diseases
138
Q

POB with restrictive disorders

A

decrease VT, decrease RR, may use different muscles to
breathe, dependent on condition

139
Q

restrictive disorders auscultation

A

decreased breath sounds

140
Q

ABG restrictive disorders

A

decrease oxygenation (PaO2)

141
Q

what characterises a restrictive disorder?

A
  • diminished lung volume
  • decreased TLC, FVC
  • normal or increased FEV1/FVC ratio
142
Q

what causes pump failure in restrictive disorders?

A
  • neural / primary muscular causes
143
Q

does restrictive disorders cause gas movement issues?

A

yes

144
Q

restrictive disorders and CO2 gas movement impairments

A

decreased gas movement if prolonged disease/ severe enough

145
Q

restrictive disorders and O2 gas movement impairments

A
  • decreased FRC
  • decreased breath size (cant get enough air in)
146
Q

how do restrictive disorders affect cough effectiveness?

A

decreases
- if inspiratory volume inadequate (cant get air in to cough)
- +/- expiratory muscles affected

147
Q

compliance definition

A

ease with which the lungs and chest wall can be expanded during inspiration

148
Q

which areas of the lung have a low compliance?

A

top (need more pressure to get air in)

149
Q

which area of the lung has higher compliance?

A

bottom (more dependent regions of the lung)

149
Q

what does reduced compliance mean?

A

the transpulmonary pressure
must change by a greater amount for a given volume
– ie, The lung/chest wall is harder to move/stiffer
– There is an increased elastic work of breathing

149
Q

what can the respiratory system compliance be affected by?

A

changes to either:
– lung compliance (elastic recoil, surfactant changes)
and/or
– chest wall compliance (joints, ligaments, muscle changes)

150
Q

skeletal disorders of the chest wall

A

– Scoliosis/kyphosis (alter joint mechanics/mm function)
– Ankylosing spondylitis (causes fibrosis and ossification of joints, including CV joints)
– Obesity (increased load from excessive soft tissue)
– Flail chest (loss of chest wall rigidity)

150
Q

obesity effect on cardiorespiratory system

A

– Reduces lung volumes, particularly ERV & FRC
– Reduces effectiveness, strength and endurance of respiratory muscles
– Increases respiratory load & effort (WOB)

150
Q

Respiratory signs and symptoms of restrictive CW disorders:
spirometry

A

restrictive pattern

151
Q

Respiratory signs and symptoms of restrictive CW disorders:
Changed POB

A

decreased VT, increased RR, asymmetrical (eg if scoliosis)

152
Q

Respiratory signs and symptoms of restrictive CW disorders:
auscultation

A

decreased breath sounds, may be asymmetrical

153
Q

Respiratory signs and symptoms of restrictive CW disorders:
ABG

A

decreased oxygenation

154
Q

chest wall compliance with scoliosis, ankylosing spondy, obesity

A

chest wall stiffer, therefore harder to expand
–> decreases compliance

155
Q

chest wall compliance with flail chest

A

Chest wall floppier
(paradoxical segment)
therefore less expansion for
same muscle effort

156
Q

DISORDERS OF THE PLEURA/ PLEURAL SPACE

A

– Pneumothorax
– Fluid in the pleural space:
effusion/haemothorax/empyema/chylothorax
– Pleural thickening

157
Q

Pneumothorax definition

A

air in the pleural space (i.e. between the visceral and parietal pleura)

158
Q

pneumothorax pathology

A

Loss of negative intrapleural pressure causes the lung
to collapse inwards

159
Q

what happens to the pleura layers in a pneumothorax

A

o visceral pleura separates from parietal, air enters IPS, air pushes/ collapses the lung down

160
Q

pneumothorax aetiology

A

Spontaneous/ primary
o Unknown cause
Secondary
o Rupture of alveoli, bulla, or blebs
Traumatic
o Penetrating injuries of the chest
o Fractured rib
o Consequence of medical emergencies

161
Q

pneumothorax symptoms

A
  • racing heart (tachycardia)
  • sudden chest pain on affected side
  • dyspnoea (increased WOB)
162
Q

pneumothorax signs

A
  • ABG decreased PaO2 (not routinely taken)
  • Dyspnoea
  • Spirometry = not done for acute conditions
  • Changed POB (muscles cant do the same amount of expansion that would normally occur at chest wall; due to decreased chest wall compliance, the POB changes)
  • Changed POB (may be asymmetrical)
163
Q

pneumothorax auscultation

A
  • Decreased/ absent breath sounds
  • pleural rub
  • bronchial breath sounds
164
Q

why arent PFT’s routinely taken acutely?

A

not a restrictive/ obstructive disorder –> disorder of chest wall

165
Q

CXR pneumothorax

A
  • increased lucency
  • lung edge visible
  • absence of lung markings
166
Q

pneumothorax impairments

A
  • restrictive airflow limitation
  • gas movement impairment (as the air outside the lung does not participate in the exchange)
  • decreased lung compliance
  • decreased chest wall compliance
  • impairments of the respiratory pump

PHTY205 (5 decks)

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