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Study Leave semester 2 year 1 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What is obstructive sleep apnoea caused by

A

Collapse of the pharyngeal airway during sleep

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2
Q

Obstructive sleep apnoea is characterised by what

A

Apnoea episodes

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3
Q

Obstructive sleep apnoea is characterised by apnoea episodes, which is what

A

Where the person will stop breathing periodically for up to a few minutes

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4
Q

Who usually reports obstructive sleep apnoea?

A

The partner- the patient is usually unaware of apnoea episodes

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5
Q

5 risk factors of sleep apnoea

A

Middle age
Male
Obesity
Alcohol
Smoking

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6
Q

Evening headache is a feature of sleep apnoea

A

No
Morning headache

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7
Q

Reduced x saturation during sleep for sleep apnoea

A

Oxygen

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8
Q

What day time features are there during the day (3)

A

Daytime sleepiness and concentration problems
Waking up unrefreshed from sleep
Morning headache

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9
Q

Severe cases of sleep apnoea can cause:

A

Hypertension
Heart failure

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10
Q

Severe cases of sleep apnoea can increase the risk of what (2)

A

Myocardial infarction
Stroke

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11
Q

What sleepiness scale is used to assess sleepiness with obstructive sleep apnoea

A

Epworth sleepiness scale

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12
Q

What daytime feature is a key feature to make you suspect obstructive sleep apnoea?

A

Daytime sleepiness
Because patients need to be fully alert for work- some occupations eg require urgent referral

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13
Q

Management of sleep apnoea? (4)

A

Referral to an ENT specialist/ specialist sleep clinic to perform sleep studies

Correct reversible risk factors

CPAP machine for continuous pressure to maintain latency of airway

Surgery final option UPPP

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14
Q

What does referral to an ENT specialist/specialist sleep clinic involve

A

(sleep in lab while monitoring O2 saturations, heart rate, resp rate, and breathing to establish any episodes and extent of snoring)

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15
Q

What are reversible risk factors of sleep apnoea

A

Alcohol
Smoking
Weight loss

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16
Q

What are the two types of restrictive lung disease?

A

Interstitial
Extra pulmonary

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17
Q

Interstitial vs extra pulmonary lung diseases?

A

Interstitial = lung tissue is damaged (hard like rubber, won’t easily allow air to enter, therefore reduce lung volume)
Extra-pulmonary = structures around lungs have been damages, so no chest expansion

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18
Q

Why does interstitial lung disease have reduced lung volume?

A

Lung material is hard and stuff like tough rubber, lung tissue won’t easily allow air in during inhalation

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19
Q

What contracts to pull the ribs up and out during inhalation?

A

The intercostal muscles and the diaphragm

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20
Q

How are the lungs pulled open when ribs are pulled up and out?

A

Cavity created in vacuum

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21
Q

What’s between alveoli

A

Connective tissue like elastin which gives the lungs their rubber-band like properties, and collagen which gives firmness and their overall shape.

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22
Q

If in interstitial lung diseases, damage occurs causing the restrictiveness, where might it come from?

A

Occupational exposures eg ASBESTOSIS

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23
Q

Where do asbestos fibres settle?

A

Lower lobes and on the pleural membrane

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24
Q

What do asbestos fibres form

A

White thick patches called pleural plaques, commonly seen on CXR

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25
Q

How is damage caused by occupational dust specifically? (2)

A

Immune reaction = immune cells damage alveolar epithelium And fibroblasts deposit ECM like collagen

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26
Q

If one type of interstitial restrictive lung disease is ‘pneumoconiosis’ ie occupational dust stuff, what another one (that’s systemic)?

A

Sarcoidosis

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27
Q

What’s happening in sarcoidosis?

A

Immune cells try to destroy pathogens and is not successful

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28
Q

Granulomas =

A

Pathogens surrounded by macrophages etc

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29
Q

Granulomas in sarcoidosis accumulate where?

A

Lymph nodes but particularly Hilum of lung

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30
Q

If severe sarcoidosis

A

Pro inflammatory cytokines = fibrosis

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31
Q

So there are three types of interstitial restrictive lung diseases:

A

Pneumoconiosis
Sarcoidosis
Hypersensitivity pneumococcus

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32
Q

Is there fibrosis in hypersensitivity pneumonitis

A

Yes lots
Chronic exposure = entire lung could be fibrotic

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33
Q

Fibrosis is what

A

Healthy lung tissue being replaced by collagen fibres

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34
Q

In restrictive , FEV1 ratio thing

A

CAN STAY THE SAME or increase
It would increase because fibrotic lung provides elastic recoil

Decreased in obstructive though

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35
Q

In interstitial restrict lung disease , what follows a decline in lung function? Mild
Severe

A

Hypoxia leading to shunt

Severe = eventually increases pulmonary hypertension
Right ventricular hypertrophy = cor pulmonale

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36
Q

Extra pulmonary restrictive lung disease, two examples?

A

1) Pleural effusion cuz of weight of fluid build up around the lungs
2) Obesity

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37
Q

Diagnosis of interstitial r lung disease? (3)

A

After cough and increasing SoB
Usually done with spirometry for FEV stuff
Imaging shows hazy whiteness in multiple lung fields = diffuse ground glass opacities

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38
Q

Treatment of interstitial restrictive lung disease

A

Corticosteroids
Immunosuppressive drugs
Anti-fibrotic therapies

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39
Q

What does remodelling mean

A
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40
Q

What are the five stages of lung development?

A

Embryonic
Pseudo glandular
Canalicular
Saccular
Alveolar

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41
Q

Embryonic lung stage

A

3-8

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42
Q

Pseudo-glandular lung stage

A

5-17 wks

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43
Q

Canalicular lung stage

A

16-26 weeks

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44
Q

Saccular lung stage

A

24-28 weeks

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45
Q

Alveolar lung stage

A

36-2/3 years

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46
Q

What happens in the embryonic stage of lung development?

A

Lung bud develops from fetal foregut
This divides into two lung buds
Then lobar buds

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47
Q

At five weeks in the embryonic stage; how many lobar buds on each side

A

3 on right, 2 on left

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48
Q

Lung buds also called,

A

Respiratory diverticulum

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49
Q

The cells lining the lung buds are derived from where

A

The endoderm

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50
Q

The blood vessels and connective tissues surrounding the lungs are derived from where

A

The mesoderm

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51
Q

What happens in the pseudoglandular stage

A

Rapid branching of the airways

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52
Q

Eventually how many segmental bronchi are formed in the pseudoglandular stage?

A

16-25 primitive segmental bronchi are formed

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53
Q

Which specialised cells appear in the airways in the pseudoglandular stage?

A

Cilia and mucous glands in the airways

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54
Q

What develops in the Canalicular stage? (Gas exchange units)

A

Terminal bronchioles
Alveolar sacs
Capillary blood vessels

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55
Q

Which special cells appear in the Canalicular stage?

A

Type 1 and type 2 celks

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56
Q

Type 1 vs type 2 cells

A

Type 1: thin membrane, allow gas exchange
Type 2: produce and store surfactant

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57
Q

Why can babies be born late stage of the canal is half stage, which is 16-26 weeks?

A

Type 1 and 2 have developed. Limit of viability
With intensive care support

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58
Q

What is the exact week for limit of viability

A

24 weeks onward

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59
Q

What happens in the Saccular stage (24-38 weeks)

A

Alveoli grow with thinner walls, more surfactant produced, bronchioles elongate

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60
Q

What happens to interstitial tissue between alveolar sacs

A

It reduces

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61
Q

What stage can sustain breathing without support

A

Final stage
‘Alveolar’
36 weeks - term and beyond

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62
Q

Alveolar sacs become what after birth

A

Alveoli

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63
Q

20-60 million air sacs at birth?

A

Yea

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64
Q

How many air sacs at 3-8 years?

A

200-300 million

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65
Q

How do we discover congenital abnormalities? (2)

A

Antenatal screening: such as ultrasound and MRI

Newborn: tachypnoea, respiratory distress, feeding issues

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66
Q

Older children may present how, if with congenital abnormalities? (4)

A

(Childhood)
Stridor/wheeze
Recurrent pneumonia
Cough
Feeding issues

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67
Q

Laryngomalacia is a congenital abnormality that presents how?

A

With stridor, worse with feeding or when upset/excited

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68
Q

What is laryngomalacia?

A

Floppiness, collapse of larynx

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69
Q

What’s tracheomalacia?

A

Abnormal collapse of tracheal walls

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70
Q

Tracheomalacia presents how? (4)

A

Barking cough
Recurrent croup
Breathless on exertion
Stridor/wheeze

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71
Q

Management of tracheomalacia?

A

Includes physio and antibiotics when unwell
Natural history, resolution with time

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72
Q

What’s the congenital abnormality tracheo-oesphageal fistula?

A

Abnormal connection between trachea and oesophagus
(Meant to just lie against each other)

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73
Q

When is tracheo-oesphageal fistula diagnosed?

A

Antenatally or postnatally- can be either

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74
Q

How does tracheo-oesphageal fistula present?

A

Choking
Colour change
Cough when feeding

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75
Q

Treatment of tracheo-oesphageal fistula?

A

Surgical repair

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76
Q

Leak and reflux, tracheomalacia, strictures are all complications found where

A

tracheo-oesphageal fistula

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77
Q

What’s CPAM? (Congenital pulmonary airway malformation)

A

Congenital pulmonary airway malformation
Is abnormal non-functioning lung tissue

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78
Q

When is CPAM usually detected?

A

80% of the time it’s detected antenatally

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79
Q

Would CPAM need surgical repair, or could it resolve spontaneously in utero?

A

Yea

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80
Q

If CPAM is asymptomatic, what then?

A

Conservative management

Surgical intervention may be required

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81
Q

Congenital diaphragmatic hernia is mostly diagnosed when

A

Antenatally

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82
Q

Congenital diaphragmatic hernia is what management?

A

Surgical repair

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83
Q

What happens after first breath?

A

Lungs inflate and fluid in lungs is absorbed

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84
Q

Transient Tachypnoea of the newborn can develop and is associated with what?

A

C section

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85
Q

Transient tachypnoea of the newborn can improve how quickly?

A

Improves within 1-2 days

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86
Q

What’s the treatment for IRDS?

A

Antenatal steroids
Surfactant replacement
Appropriate ventilation

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87
Q

What is chronic lung disease associated with? And what’s required?

A

Prematurity, ongoing oxygen requirement at term

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88
Q

What’s remodelling?

A

Alteration of airway structure following external influence

89
Q

3 reasons why remodelling might occur?

A

Environmental exposures
Chronic diseases of childhood
Infection

90
Q

How might remodelling lead to abnormalities?

A

Due to interference of inter-cellular signalling

91
Q

Remodelling is never seen in asthma, only chronic lung disease of prematurity

A

False
Remodelling is also seen in asthma

92
Q

How come remodelling is seen in asthma? (4)

A

Chronic inflammation, therefore:
Increased bronchial responsiveness
Increase mucus secretion
Airway oedema
Airway narrowing

93
Q

Lung function deficits that are established by school age, May track into adult life? And increase risk of what?

A

Yes
Increase risk of adult lung obstructive diseases, such as COPD

94
Q

What is this describing: ‘200 + diseases causing thickening of the interstitium, and can result in pulmonary fibrosis

A

ILD

95
Q

What is a typical presentation of idiopathic pulmonary fibrosis?

A

Chronic breathlessness and cough
Typically 60-70 years old, commoner in men
Clubbed and crackles

96
Q

Median survival of idiopathic pulmonary fibrosis?

A

3 years

97
Q

Treatment options for idiopathic pulmonary fibrosis?

A

Oral anti-fibrotic - pirfenidone, nintedanib, palliative care

Surgical option: transplant

98
Q

What type of genetic disorder is cystic fibrosis?

A

An autosomal recessive disorder

(Of the CFTR gene, on chromosome 7)

99
Q

Both father and mother need to have the CFTR gene for CF to happen

A

Yah

100
Q

What’s CFTR?

A

A channel that pumps chloride ions into secretions

101
Q

In newborns with CF, why is lots of extra mucus bad

A

Meconium- first stool- gets thick and sticky… therefore may get stuck in intestines and not come out , and is called meconium ileus, and is a surgical emergency

102
Q

What is meconium ileus?

A

Meconium- first stool- gets thick and sticky… therefore may get stuck in intestines and not come out ,

103
Q

In early childhood, what’s the most prominent affect of CF? And why

A

Pancreatic insufficiency

Thick secretions block the pancreatic duct
So not a lot of digestive enzymes make it to the intestines

104
Q

Affect of pancreatic insufficiency, where there are no pancreatic enzymes in the intestines?

A

No proteins or fat is absorbed
Therefore poor weight gain, and failure to thrive

105
Q

What steatorrhea, and why in CF

A

If pancreatic insufficiency, fat and proteins not absorbed, so we have fat containing stools

106
Q

Why might the pancreas be damaged?

A

Because backed up pancreatic enzymes attack the pancreas

(Maybe inflammation and therefore acute pancreatitis)
And therefore chronic pancreatitis

107
Q

Why is cystic fibrosis called cystic fibrosis

A

Because backed up pancreatic enzymes attack the pancreas

(Maybe inflammation and therefore acute pancreatitis)
And therefore chronic pancreatitis

And therefore cysts develop- cystic fibrosis

108
Q

Why diabetes in CF?

A

Destruction of pancreatic tissue = compromise endocrine function of the pancreas…Causing insulin-dependant diabetes

109
Q

When do lung problems for Cf crop up

A

Usually later in childhood

110
Q

In CF what’s wrong with cilia

A

Mycolciliary ladder are defective cause thick, so bacteria builds,
Therefore
Symptoms like cough and fever

111
Q

CXR issue that prompts

A

Increased bacterial load = CF exacerbation,
So prompts a round of antibiotics

112
Q

Example of CF exacerbation?

A

Pneumonia

113
Q

Staphylococcus aureus could never be an issue in CF

A

Wrong

114
Q

How get bronchiectasis in CF

A

Chronic bacterial infection and inflammation

115
Q

What is bronchiectasis?

A

Airway wall damage, causing permanent dilation of the bronchi

Possibly haemoptysis

116
Q

Why respiratory failure in CF? (And therefore death)

A

Repeated CF exacerbations

117
Q

Digital clubbing might occur in what

A

CF

118
Q

Infertility in CF might only occur in women

A

No also men

119
Q

What are nasal polyps

A

Tissue growths in the nose that might occur in CF

120
Q

What’s ABPA that might occur in CF?

A

Allergic bronchopulmonary aspergillosus

Which is a hypersensitivity reaction to the fungus aspergillosis fumigatus, which can live in a sinus or lung cavity

121
Q

Diagnosis for CF- to confirm

A

Newborn screening- detects IRT (immune reactive trypsinogen) which gets released into the blood when pancreas is damaged

Sweat test for high levels of chloride (in sweat… vs rest of body where chloride can’t get back in)

122
Q

Treatment for CF, nutrition and weight gain (3)

A

Fat soluble vitamina
Replacement pancreatic enzymes
Extra calories

123
Q

What’s the CF pulmonary treatment?

A

Chest physiotherapy- banging on chest basically
Inhalers

124
Q

What CF medications?

A

Meds like n acetylcysteine that cleaves bonds in mucus glycoproteins, or cuts up nucleus acid in mucus to thin it out

125
Q

What to monitor disease in CF

A

Pulmonary function test

126
Q

Ultimate treatment in CF

A

Lung transplant

127
Q

Why personalised treatments

A

To target specific CFTR mutation types

128
Q

What is a lung abscess?

A

A collection of pus surrounded by granulation tissue?

129
Q

Why do lung abscesses occur? (5)

A

Aspiration (often cause of pneumonia)
(Maybe drunk, or tooth, or child, or epilepsy seizure = mistake)

Infection causes necrosis

130
Q

What tends to happens to lung abscesses?

A

Empyema: They have a tendency to rise to surface of the organ and discharge pus eg bursts into the pleural cavity and causes pus to form in the pleural space

131
Q

What’s empyema

A

Pus in pleural space

132
Q

With pneumonic patient… patient suddenly experiences sudden onset of severe chest pain, which is pleuritic in nature = what

A

Onset of pyogenic empyema

133
Q

If leakage of pus is very localised, would still be considered a lung abscess vs if spread through whole pleural cavity, it’s called:

A

Empyema (or empyema thoracis)

134
Q

What might happen post operative, following an infection that progresses into the chest

A

Empyema

135
Q

Following infection, with fibropurulent covering, and loads of pus, stops kings doing what

A

Expanding

136
Q

What’s decortication

A

Surgical removal of the surface layer, membrane, or fibrous cover of an organ

137
Q

Why would decortication happen

A

When the lung is covered by a thick, I elastic pleural peel restricting lung expansion

138
Q

What’s a pleurectomy

A

Peeling the parietal pleura off the chest wall

139
Q

What are thymic tumours linked to

A

Myasthenia gravis

140
Q

Are thymomas always malignant?

A

Yes

141
Q

Thymic carcinoma is the worst thymic tunour

A

Yes

142
Q

Why are thymic tumours so bad?

A

They tend to invade locally into surrounding structures, such as the heart, great vessels, aortic arch

143
Q

When could you operate on a thymic tumour, when they invade where?

A

Invade into the superior vena cava, and travel within the lumen of the entry to vena cava

Therefore
Do a sternotomy and remove them - have a very close resection margin

144
Q

Why might thymic tumours have adjuvant chemotherapy, or radiotherapy after surgery?

A

They have a very close resection margin

We follow them for 5 years

145
Q

Are thymomas responsive to chemo and radiotherapy?

A

Yes

146
Q

Prognosis for thymomas vs carcinoid tumours?

A

Thymomas have okay prognosis
Carcinoid tumours are frequently not curable by surgery, and tend to reoccur

147
Q

Is tracheal surgery common?

A

Not at all

148
Q

When might you do tracheal surgery?

A

If an iatrogenic injury has occurred during another surgery, so might have to operate on the trachea to repair the tear and put it back together

149
Q

Primary or secondary pneumothorax?

A

Primary = no underlying, might just be one portion e.g. apex
Secondary = widespread pathology throughout the lungs eg COPD or pulmonary fibrosis

150
Q

Pneumothoraxes are often secondary to what (2)

A

COPD
Pulmonary fibrosis

151
Q

Would you usually operate on a secondary pneumothorax

A

Nah
But yea for primary

152
Q

Pneumothorax often results in what

A

Lung collapse

153
Q

Tension pneumothorax is often associated with what

A

Air travel
And diving
Because these situations cause changes in the atmospheric pressure which contributes to the ethology of the pneumothorax in those cases

And often causes bilateral pneumothorax

154
Q

How many of those with a haemopneumothorax, will the bleeding just stop?

A

About 50%

155
Q

For a haemopneumothorax where it just continues to bleed?

A

Be operated on in order to cauterise the bleeding point on the chest wall, to carry out the necessary surgery to prevent recurrence of pneumothorax

156
Q

What’s bulbous lung disease?

A

Very large abnormal air space in the lungs
A bulls is defined as ‘abnormal air space within the lung’ MORE THAN 2cm in diameter.

157
Q

Bullae typically occur in which people

A

Smokers

158
Q

People with bullae can’t wait

A

Fly

Could double in size, cause a pneumothorax to develop, or cause tearing of the pulmonary veins around the wall of the bulla

159
Q

A pulmonary embolism is a type of what

A

Pulmonary vascular disease

160
Q

Pulmonary hypertension is a type of what disease

A

Pulmonary vascular disease

161
Q

Is cancer a risk factor for venous thromboembolism?

A

Yes
Partly a clotting factor mechanism
Partly mechanical e.g. if you’ve got a tumour in the abdomen, pressing on veins, then obviously flow in the veins is reduced

162
Q

Why pregnancy risk for venous thromboembolism

A

Pregnant =
Clotting factors
Fetus pressing on veins

163
Q

Thrombophilia predisposes you to what?

A

Thrombosis

164
Q

3 groups of symptoms for pulmonary embolism depending on the size?

A

Pleuritic chest pain, cough and haemoptysis

Isolated acute dyspnoea

Syncope or cardiac arrest if massive PE

165
Q

Signs of pulmonary embolism based on severity:

A
  1. Pyrexia, pleural rub, stony dullness to percussion at base (pleural effusion)
  2. Tachycardia, tachypnoea, hypoxia
  3. Tachycardia, hypotension, tachypnoea, hypoxia
166
Q

Why is transient pyrexia a sign of pulmonary embolism?

A

Well part of the lung tissue has infarcted

167
Q

What sound might you hear with a pulmonary embolism?

A

A pleural rub

168
Q

Do you always get a pleural effusion with pulmonary embolism?

A

No

169
Q

If you suspect a pulmonary embolism, what is it important to do?

A

Try and assess the risk or likelihood of pulmonary embolism before you do any tests
These are:
Wells score (includes symptoms and signs of VTE, previous VTE and risk factors)
Revised Geneva score
Based on risk factors, symptoms and signs (heart rate)

170
Q

For the wells score, what number suggests suggest PE is unlikely to likely:

A

0-4 points is unlikely
>4 points is likely

171
Q

Would you do a fbc for PE?

A

Yah

172
Q

Would you do CXR for pulmonary embolism?

A

Yh
Though CXR often looks normal, although sometimes you can have subtle abnormalities

173
Q

In the acute stage, would the CXR of a PE more likely to look normal or not?

A

CXR looks normal often at acute stage

174
Q

What would an ECG show in a pulmonary embolism?

A

Sinus tachycardia

175
Q

What’s a d dimer- low?

A

If low or negative, pulmonary embolism very unlikely

176
Q

If you’ve got a low wells score and a negative d-dimer?

A

You could reasonably discount pulmonary embolism as a diagnosis

177
Q

Would you ever do a CT pulmonary angiogram for PE?

A

Yeah

178
Q

What would you see in V/Q scan for pulmonary embolism?

A

Absence of perfusion is due to pulmonary embolism

179
Q

Treatment of hypoxic patient in PE?

A

Oxygen

180
Q

If PE is strongly suspected, what treatment?

A

Low molecular weight heparin in a therapeutic dose- even before CT scan

181
Q

What’s heparin

A

Anticoag

182
Q

If a massive pulmonary embolism, patient is shocked, what treatment might you give?

A

Thrombolysis

183
Q

Would you give both thrombolysis and low molecular weight heparin?

A

Ideally not

184
Q

Ideally low molecular weight heparin for pulmonary embolism, or thrombolysis?

A

Low

185
Q

If massive PE then what

A

Def thrombolysis

186
Q

What does thrombolysis do

A

Dissolve the clot essentially

187
Q

What’s a pulmonary embelectomy

A

It’s a surgical procedure

188
Q

Idiopathic pulmonary arterial hypertension typically presents in which people?

A

Young adults

189
Q

Pulmonary hypertension eventually leads to what heart failure?

A

Right

190
Q

Would pulmonary hypertension ever be secondary to left sided heart disease

A

Yeah
Eg mitral stenosis

191
Q

Could you get pulmonary hypotension secondary to any chronic respiratory disease? Which ones for example?

A

Yea
Eg severe COPD, sleep apnoea, interstitial lung disease,
Shunt you see

192
Q

What could repeated pulmonary embolisms lead to?

A

Pulmonary hypertension

193
Q

4 symptoms of pulmonary hypertension?

A

Exertions dyspnoea
Chest tightness
Exertion all presyncope or syncope
Haemoptysis

194
Q

Signs of pulmonary hypertension

A

Elevated JVP
Right ventricular heave
Loud pulmonary secondary heart sound
Hepatomegaly
Ankle oedema

195
Q

Why elevated JVP in pulmonary hypertension?

A

Cuz rig by ventricle dilated, not contracting properly, then the pressure will build up in the venous system, and you’ll get an elevated jugular venous pressure

196
Q

Why might you feel a ventricular heave in pulmonary hypertension?

A

Maybe due to failure of the right ventricle

197
Q

Investigations for pulmonary hypertension.

A

ECG
Lung function test
CXR
Echocardiography
V/Q scan

198
Q

What’s the most important pulmonary hypertension investigation probs

A

Echocardiography

199
Q

What’s right heart catheterisation (might do to confirm pulmonary hypertension)

A

Putting a plastic tube in the groin or neck, put catheter through the right atrium, right ventricle, into the pulmonary artery. To get MAP

200
Q

What’s Doppler test for p hypertension

A

Often tricuspid valve leaks a bit
So can use Doppler physiology to measure the velocity of that leak

201
Q

General treatment of pulmonary hypertension?

A

Treat underlying condition
Oxygen
Anticoagulant
Diuretics

202
Q

When might you use calcium channel antagonists?

A

If positive vasodilator trial, for pulmonary hypertension

203
Q

What’s the positive vasodilator test for calcium channel antagonists

A

See if patient will respond to calcium channel antagonists

204
Q

What’s narcolepsy?

A

When the brain is unable to regulate sleeping and waking patterns normally, which can result in: excessive daytime sleepiness and sleep attacks- falling asleep suddenly and without warning

205
Q

What are the 5 signs of narcolepsy?

A

Excessive daytime sleepiness
Sudden loss of muscle tone/ cataplexy
Sleep paralysis
Hallucinations
Changes in REM sleep

206
Q

What’s cataplexy

A

Temporary loss of muscle control resulting in weakness and possible collapse, often in response to emotions such as laughter and anger

207
Q

PaCO2 May be low in type 1 respiratory failure

A

True

208
Q

Which type of respiratory failure is most common?

A

Type 1

209
Q

Type 1 resp failure results from failure of what?

A

Failure of oxygenation only
Problem with 1 gas only

(Type 1 = problem with 1 gas, type 2 = problem with 2 gases)

210
Q

In a normal lung, the interstitium is made up of fibrous tissue between the basement membranes of the alveolar epithelium and the capillaries

A

False

In a healthy lung, the alveolar wall and the surrounding capillaries are in direct contact, to allow efficient gas diffusion and exchange

211
Q

Why haemoptysis in CF

A

(Often) caused by destruction of the bronchial walls through the CF disease process

212
Q

Narcolepsy is associated with delayed onset of REM sleep

A

False
It is associated with rapid onset of REM sleep, and hallucinations at the time of falling asleep and/or waking

213
Q

Hypoxaemia due to a large shunt does not respond well to supplementary oxygen

A

Increasing the oxygen concentration in the alveoli will therefore have no impact on the oxygenation of the blood

214
Q

Congenital pulmonary airway malformation can occasionally be associated with risk of malignant change

A

True

215
Q

Epworth sleepiness score of what or more is considered abnormal?

A

A score of 11 or more is abnormal

216
Q

Idiopathic pulmonary hypertension is common

A

False
Very rare

217
Q

What does an opiate overdose do?

A

Suppress respiratory drive, and cause type 2 respiratory failure by causing alveolar hypoventilation

218
Q

What does diffuse alveolar damage occur from?

A

Results from acute lung injury/inflammation

Incl. chemical injury, respiratory viruses incl covid, drug effects, major trauma

219
Q

Gas exchange units form when during development

A

Canalicular

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