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y1systems > Week 5 resp > Flashcards

Week 5 resp Flashcards

1
Q

Describe restrictive lung complaince in terms of FEV1, FVC and their ratio

A

Low FEV1 and LOW FVC but FEV1/FVC is normal ratio

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2
Q

What is the interstitum?

A

The connective tissue space around the airways and vessels - The space between the basement membranes of the alveolar walls

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3
Q

What material reduces the compliance of the lung and impaedes the elasticity of the alveoli?

A

Collagen

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4
Q

Describe the characteristics of restrictive lung disease

A

Reduced gas transfer
Diffusion abnormalities
Ventilation/Perfusion imbalances
small airways are affected by pathology

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5
Q

Is there airflow limitation in restrictive lung disease

A

Nope

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6
Q

What are the clinical presentations for restrictive lung disease

A

Discovery of abnormal CXR
Dyspnoea
resp failure - type 1
HF

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7
Q

What are 3 chronic outcomes from a parenchymal (intersitial) lung injury

A

Usual interstitial pneumonitis
Granulomatous responses
Other patterns

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8
Q

What does DAD stand for?

A

Diffuse alveolar damage

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9
Q

What is DAD associated with?

A 
major trauma
Chemical injury/toxic inhalation
Circulatory shock
Drugs
Infection
Autoimmune disease
Radiation
However can still be idiopathic
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10
Q

Describe the exudative stages of DADs

A

within first 7 days
Oedema and hyline membranes
- Oedema: arises immediately. vessels become massively leaky, moreso than in a normal response (typically gone by day 3)
- Hyline membranes: arise after a day, decreased to half its peak value by 7 days. Contain lots of proteins

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11
Q

Describe the proliferative stage of Dads

A

A combination of interstitial fibrosis and interstitial inflammation

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12
Q

What are the histological features of DADs

A

Protein rich oedema
Fibrin
Hyaline membranes
Denuded basement membranes

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13
Q

What is the most common interstitial lung disease?

A

Sarcoidosis

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14
Q

Apart from sarcoidosis what is the other granulomatous response?

A

Hypersensitivity pneumonitis

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15
Q

Describe the histopathology of sarcoidosis

A

Epitheloid and giant cell granulomas
necrosis/Caseation very unusual - Differentiates from TB
Little lymphoid infiltrate
Variable associated fibrosis

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16
Q

Describe the presentation of sarcoidosis

A
  1. Young adult: Acute arthralgia, arythema nodosum, Bilateral hilar lymphadenopathy
  2. Incidental Abnormal CXR: No symptoms
  3. SOB, cough and abnormal CXR
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17
Q

What is the treatment for sarcoidosis

A

Corticosteroids

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18
Q

Describe the acute presentation for hypersensitivity pneumonitis

A

Fever, dry cough, myalgia
Chills, 4-9 hours after Ag exposure
Crackles, tachypnoea, wheeze
Precipitating antibody

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19
Q

What is the chronic presentation of hypersensitivity pneuomonitis

A

Malaise, SOB, Cough
Low grade illness
Crackles and some wheeze
[Can lead to rep failure, gas transfer low, history important]

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20
Q

What type of hypersensitivity causes hypersensitivity pneuomnitis?

A

immune complex mediated combined Type II and Type IV hypersensitivity reaction

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21
Q

Hypersensitivty pneumonitis is said to cause Bronchiolitis obliterans, what does this mean?

A

Inflammatory obstruction of bronchioles, these bronchioles become damaged and ingflamed by chemical particles or respiratory infections. Features extensive scarring that blocks airways.

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22
Q

What are the casues of usual interstitial pneomonitis?

A 
Connective tissue diseases: scleroderma and rheumatoid disease
Drugs
Asbestos
Viruses
Idiopathic/Cryptogenic reasons
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23
Q

Describe the interstitium of a patient with UIP

A

Patchy chronic inflammation
Type 2 pneumocytes hyperplasia
Smooth muscle and vascular proliferation
Proliferating fibroblastic foci

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24
Q

What are Proliferating Fibroblastic Foci

A

nodules of fibrous tissue in the walls of the alveoli, reflect the severity of the disease

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25
Q

What is the clinical presentation of idiopathic pul fibrosis?

A

Dyspnoea, cough

Basal crackles, cyanosis, clubbing

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26
Q

Prognosis for idiopathic pul fibrosis?

A

<5 years

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27
Q

Describe type 1 resp failure

A

PaO2 <8kPa (PaCO2 normal or low)

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28
Q

Describe type 2 resp failure

A

PaCO2 >6.5 kPa (PaO2 usually low)

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29
Q

What is the resut of alveolar hypoventilation on PACO2 and PAO2 ?

A

Hypoventilation increases the PACO2 and therefore decreases PaCO2

Increased PACO2 takes up space in the alveoli and therefore causes PAO2 and PaO2 to fall

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30
Q

How can you correct a fall in PaO2 due to hypoventilation?

A

Raising the FIO2

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31
Q

What is the commones cause of hypoxaemia clinically?

A

V/Q mismatch

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32
Q

Why is normal V/Q ration 0.8?

A

Normally breath 4 l/min. CO is 5 l/min so normal V/Q is 4/5 or 0.8

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33
Q

How can you treat hypoxaemia due to low V/Q?

A

Increase in FIO2

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34
Q

What are the pleural cases of restrictive lung disease

A

Pleural effusion
Pneumothorax
Pleural thickening - asbestos related pneumonia

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35
Q

What are the skeletal causes of restrictive lung diseases

A

Kyphoscoliosis
Ankylosing spondylitis
Thoracoplasty
Rib fractures- soreness

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36
Q

What are the muscular causes of restrictive lung disease

A

Amyotrophic lateral sclerosis
Obesity - sub diaphragmatic - diaphragm can’t fall properly
Pregnancy - sub diaphragmatic

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37
Q

What is sarcoidosis?

A

Multisystem granulomatosus disease of unknown cause

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38
Q

What is the histological hallmark of sarcoidosis

A

Non-cesating granuloma

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39
Q

What are the clinical signs of sarcoidosis

A

Eythrma nodosum

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40
Q

Typically who gets sarcoidosis?

A

Adults < 40
Women > men
World wide

41
Q

When would you treat sarcoidosis with NSAIDS?

A

Erythema nodosum/arthralgia

42
Q

When would you treat sarcoidosis with Topical steroids?

A

Skin lesions/anterior uveitis/Cough

43
Q

When would you treat sarcoidosis with systemic stroids?

A

Cardiac, neurologica, eye disease not responding to topical Rx, hypercalcaemia

44
Q

What is the typical presentation for idiopathic pul fibrosis

A

Crhonic SOB and cough
Typically 60-70 years old, commoner in men
Failed Rx for LVF or infection
Clubbed and crackles

45
Q

How does fibrotic tissue vary in the lung?

A

Usually most prominent in the peripheral tissue, central tissue is usually unaffected- worsens as severity of the condition increases

46
Q

How do large shunts respond to increases in FlO2?

A

Poorly, dont do it pal

47
Q

What is FLO2?

A

The fraction of inspired air which is oxygen

48
Q

Define obstructive sleep apnoea

A

Recurrent episodes of upper airway obstruction leading to apnoea during sleep

49
Q

Describe the presentation of obstructive sleep apnoea

A

Usually associated with heavy snoring
Typically un-refreshing sleep
Daytime somnolenece/Sleepiness
Poor daytime concentration

50
Q

What score in the epworth questionare is considered abnormal?

A

11 or higher

51
Q

Describe the severity of sleep apnoea with reference to the desaturation rate/AHI

A

0-5: normal
5-15: Mild
15-30: Moderate
>30: severe

52
Q

Describe the treatment for sleep apnoea

A

Identify and discourage exacerbating factors (wieght, alcohol)
diagnose and treat possible endocrine disorders
Mandibular repositioning splint

53
Q

Define narcolepsy

A

A chronic sleep disorder characterised by overwhelming daytime drowsiness and sudden attacks of sleep

54
Q

What are the clinical features of narcolepsy

A

Cataplexy - where person suddenly collapses and seems to be asleep but is aware of what is going on around them
Excessive daytime somnolence
Hypnagogic/Hyponopomic hallucinations
Sleep paralysis

55
Q

What is the treatment for narcolepsy

A

Modafinil
Dexamphetamine
Venlafzine
Sodium Oxybate

56
Q

Define chronic ventilatory failure

A

Defined by the following factors:

  • elevated pCO2 (>6kPa)
  • PO2 <8kPa
  • Normal blood pH
  • Elevated bicarbonate (HC03)
57
Q

What are the symptoms of chronic ventilatory failure

A 
SOB
Orthopnoea
Ankle swelling
Morning headache
Reccurent chest infections
Disturbed sleep
58
Q

What are the 5 stages in the normal growth and development of the lungs

A 
Embryonic
Pseudoglandular
Canalicular 
Saccular
Alveolar
59
Q

Describe the embryonic stage of lung development

A

3-8 weeks

  • Lung bud starts to develop as resp diverticulum from the foetal foregut
  • At 5 weeks 2 primary lung buds visible
  • Later divide into lobar buds (3 on right 2 on left)
  • Like cell from gut, derived from endoderm
  • Blood vessels and stuff are derived from endoderm
60
Q

Describe the pseudoglandular stage of lung development

A

5-17 weeks

  • Rapid branching of airways
  • will be 16-25 primitive segmental bronchi which will continue to elongate and wider in later phases
  • Development of specialised cells (cillia)
61
Q

Describe the Canalicular stage of lung development

A

16-26 weeks

  • When lungs develop distal architecture
  • Terminal bronchiole, alveolar sacks and capillaries form gas exchange units
  • Type 1 and 2 pneumocytes are formed
  • In later stages, presence of gas exchange units make possible for premature delivery and survive with support - described as the limit of viability
62
Q

Describe the Saccular stage of lung development

A

24-38 weeks

  • Bronchioles elongate and interstitial tissue between sacs reduce
  • Alveolar sacs grow in size and become well formed
  • More surfactant is produced
  • Alveolar walls become thinner
63
Q

Describe the alveolar stage of lung development

A

36 weeks, term and beyond

Can sustain breathing without support

64
Q

Describe laryngomalacia

A

Floppiness of airway - Dynamic abnormal collapse of voicebox

  • Commonly seen in infants
  • Presents with stridor, worse with feeding when upset/excited
  • Will improve within first year
  • Concern if affects feeding, growth or causes apnoeas
65
Q

Describe tracheomalacia

A

Floppiness of trachea

  • Can be isolated in healthy infants
  • Associated with genetic conditions
  • May be caused by external compression
66
Q

Describe the presentation of tracheomalacia

A
  • Barking cough
  • Recurrent ‘croup
  • Breathless on exertion
  • Stridor/wheeze
67
Q

Describe the management of tracheomalacia

A

Includes physio and abx when unwell

Natural history resolution within time

68
Q

Describe a tracho-oesphagoeal fistula

A
  • Abnormal conenction between trachea and oesophagus
  • Majority have associated oesophageal atresia
  • Associated with genetic conditions
  • May be diagnosed anteneally or postnatally
69
Q

What is the presentation of a tracho-oesphagoeal fistula

A
  • Choking
  • Colour change
  • Cough with feeding
  • Unable to pass NG
70
Q

What is the treatment of a tracho-oesphagoeal fistula

A
  • Surgical repair
  • Complications include:
    tracheomalacia
    Strcutres due to narrowing of oesophagus
    Leak
    Reflux
71
Q

Describe congenital pulmonary airway malformations

A

Abnormal non functioning lung tissue

  • 80% detected antenatally
  • Occur sparodically
  • May resolve in utero
  • Conservative management if asymptomatic
  • Surgical intervention may be required
  • Possible risk of malignant change
72
Q

Describe a conegntial diaphragmatic hernia

A

= when diaphragm doesnt close

  • CDH affects 1 in 2500 births
  • Usually left side > right side
  • Most diagnosed antenatally
  • Some cases diagnosed late
  • Managment = surgical repair
  • Prognosis depends on degree of lung hpoplasia
73
Q

Describe the genetics of CF

A

Single gene disorder - autosomal recessive - most common in caucasians

74
Q

How many people ae carriers of CF?

A

1 in 25 people

75
Q

How does CF occur?

A

Due to mutation in the transmembrane conductance regular protein which is coded on chromosome 7

76
Q

What is the implications of abnormal transport of chloride and sodium?

A
  • reduced airway surface liquid
  • Thick sticky mucous
  • Shearing
  • Impaired bacterial killing via neutrophils
77
Q

How many classes of Cf are there?

A

6

78
Q

Describe the 6 classes of CF

A

Class 1-3 is severe deisease

Class 4-6 is milder

79
Q

Describe the antenatal testing methods in CF

A

= Preimplantation genetic diagnosis
Chorionic villous sampling
Amniocentesis

80
Q

Describe the neonatal screening for CF

A 
Nowborn bloodspot (day 5_ - Gurthie test
Sweat testing
- measures onc. of chloride excreted in sweat elevated in CF
- Tests usually repeated to confirm
- Less reliable in adults
81
Q

Describe the parameters of the results of a sweat test for CF

A

30-59 = inconclusive
<30 in infant over 6 months old = probably not CF
60 or over = CF

82
Q

What are the different systems affected by CF?

A

Pancreatic insufficiency
Diabetes
Lung infection and bronchiectasis

83
Q

Describe pancreatic insuffiency within CF

A

The pancreas produces enzymes that digest food. lack of these enzymes leads to malabsorption, abnormal stools and a general failure to thrive girlie.

  • There are 6 classes of CF - thus 6 levels of pancreatic function
  • Class 1-3 are pancreatic insufficient
  • Class 4-6 have some pancreatic function
  • Only need about 5% of CFTR function to have sufficient function and be asymptomatic
84
Q

Describe what reccurrent chest infections may occur as a result of CF

A

Pneumonia
Bronchiectasis
Scarring
Abscesses

85
Q

Why do pulmonary infections occur in CF?

A
  • There is abnormal electrolyte transport across the cell membrane
  • Dehydration of airway surface layer (water layer which allows muccous of to slide easily up airway to be coughed up
  • Thus there is a decreased mucocillary clearance
  • Mucous sticks to mucosal surface and causes shearing damage
  • This causes increased bacterial adherance and decreased bacterial killing
86
Q

What is the overarching effect of reccurent resp infections in CF

A

Cause progressive respiratory decline due to progressive bronchiectasis -> chronic sputum production

87
Q

Is nail clubbing present in CF

A

It CAN BE

88
Q

Describe the management of pancreatic insufficiency in CF

A
  • Need to boost nutrition
  • Can replace enzymes with CREON -> need to tkae 30-40 per day so tend to dak handful with meals
  • Given high energy diet plus calorie supplement drinks
  • Given nutritional suppliments: Fat soluble vitamin and mineral supplements
89
Q

Describe the management of the respiratory features of CF

A
  • Mucous obstruction inflammation: Airway clearance via physiotherapy, mucolytics and bronchodilators
  • Chronic infection: abx
  • Increased inflammation: Azithromycin
  • Fibrosis/Scarring/Bronchiectasis: supportive treatment and management of symptoms
90
Q

What are other aspects of CF

A

Diabetes
Osteoporosis
Pneumothorax
Haemoptysis

91
Q

Describe the aspect of diabetes in CF

A
  • type of diabetes and management differs from non CF patients
  • Joint diabeteic/CF clinicls and CF dietician vital
  • Type 2 is the commonest type seen in CF
    [not enough insulin from pancreas or insulin not working properly]
  • type 1 is very rare in CF
    [no insulin made]
92
Q

Describe the aspect of osteoporosis in CF

A
  • BMD falls in patients with CF
  • Slower gain, faster loss, worse the sicker you are
  • increased risk of fractures
  • May exclude lung transplant
  • Treatement = bone protection drugs, wieght bearing exercises
93
Q

Describe haemoptysis as an aspect of CF

A

= Bronchial wall destruction causing coughing up of blood

  • Minor haemoptysis is very common (60%) - blood streaking, no specific treatment
  • Massive haemoptysis in 1% of pts each year: May be preceded by ‘gurgling’ in chest. Admit patients with this and resus. May need bronchial angiogram and embolisation
94
Q

Describe the pathophysiology of a pul embolism

A

Thrombus form sin the venous system. usually in deep veins of the legs and embolisms to the pulmonary arteries

95
Q

What are the symptoms for a pulmonary embolism

A

pleuritic chest pain, cough and haemoptysis
Isolate acute dysponea
Syncope or cardiac arrest (MASSIVE PE)

96
Q

What are the signs of a PE

A
  1. Pyrexia, pleural rub, stony dullness to percussion at base (pleural effusion)
  2. Tachycardia, tachypnoea, hypoxia
  3. Tachycardia, hypotension, tachypnoea, hypoxia
97
Q

What is the treatment for PE

A

Oxygen
Low molecule weight heparin eg dalteparin
Warfarin
Direct oral anticoagulants (DOAC): Rivaroxaban, apixaban
Thrombolysis: Alteplase (rt-PA)
Pulmonary embolectomy

98
Q

What is pulmonary hypertension

A

Elevated blood pressure in the arterial tree
Defined as a mean pul artery pressure of >25mmHg
Either primary or secondary to other conditions

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