Week 5 Flashcards
1
Q
What is obstructive sleep apnoea caused by
A
Collapse of the pharyngeal airway during sleep
2
Q
Obstructive sleep apnoea is characterised by what
A
Apnoea episodes
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
4
Q
Who usually reports obstructive sleep apnoea?
A
The partner- the patient is usually unaware of apnoea episodes
5
Q
5 risk factors of sleep apnoea
A
Middle age
Male
Obesity
Alcohol
Smoking
6
Q
Evening headache is a feature of sleep apnoea
A
No
Morning headache
7
Q
Reduced x saturation during sleep for sleep apnoea
A
Oxygen
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
9
Q
Severe cases of sleep apnoea can cause:
A
Hypertension
Heart failure
10
Q
Severe cases of sleep apnoea can increase the risk of what (2)
A
Myocardial infarction
Stroke
11
Q
What sleepiness scale is used to assess sleepiness with obstructive sleep apnoea
A
Epworth sleepiness scale
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
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
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)
15
Q
What are reversible risk factors of sleep apnoea
A
Alcohol
Smoking
Weight loss
16
Q
What are the two types of restrictive lung disease?
A
Interstitial
Extra pulmonary
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
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
19
Q
What contracts to pull the ribs up and out during inhalation?
A
The intercostal muscles and the diaphragm
20
Q
How are the lungs pulled open when ribs are pulled up and out?
A
Cavity created in vacuum
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.
22
Q
If in interstitial lung diseases, damage occurs causing the restrictiveness, where might it come from?
A
Occupational exposures eg ASBESTOSIS
23
Q
Where do asbestos fibres settle?
A
Lower lobes and on the pleural membrane
24
Q
What do asbestos fibres form
A
White thick patches called pleural plaques, commonly seen on CXR
25
How is damage caused by occupational dust specifically? (2)
Immune reaction = immune cells damage alveolar epithelium And fibroblasts deposit ECM like collagen
26
If one type of interstitial restrictive lung disease is ‘pneumoconiosis’ ie occupational dust stuff, what another one (that’s systemic)?
Sarcoidosis
27
What’s happening in sarcoidosis?
Immune cells try to destroy pathogens and is not successful
28
Granulomas =
Pathogens surrounded by macrophages etc
29
Granulomas in sarcoidosis accumulate where?
Lymph nodes but particularly Hilum of lung
30
If severe sarcoidosis
Pro inflammatory cytokines = fibrosis
31
So there are three types of interstitial restrictive lung diseases:
Pneumoconiosis
Sarcoidosis
Hypersensitivity pneumococcus
32
Is there fibrosis in hypersensitivity pneumonitis
Yes lots
Chronic exposure = entire lung could be fibrotic
33
Fibrosis is what
Healthy lung tissue being replaced by collagen fibres
34
In restrictive , FEV1 ratio thing
CAN STAY THE SAME or increase
It would increase because fibrotic lung provides elastic recoil
Decreased in obstructive though
35
In interstitial restrict lung disease , what follows a decline in lung function? Mild
Severe
Hypoxia leading to shunt
Severe = eventually increases pulmonary hypertension
Right ventricular hypertrophy = cor pulmonale
36
Extra pulmonary restrictive lung disease, two examples?
1) Pleural effusion cuz of weight of fluid build up around the lungs
2) Obesity
37
Diagnosis of interstitial r lung disease? (3)
After cough and increasing SoB
Usually done with spirometry for FEV stuff
Imaging shows hazy whiteness in multiple lung fields = diffuse ground glass opacities
38
Treatment of interstitial restrictive lung disease
Corticosteroids
Immunosuppressive drugs
Anti-fibrotic therapies
39
What does remodelling mean
40
What are the five stages of lung development?
Embryonic
Pseudo glandular
Canalicular
Saccular
Alveolar
41
Embryonic lung stage
3-8
42
Pseudo-glandular lung stage
5-17 wks
43
Canalicular lung stage
16-26 weeks
44
Saccular lung stage
24-28 weeks
45
Alveolar lung stage
36-2/3 years
46
What happens in the embryonic stage of lung development?
Lung bud develops from fetal foregut
This divides into two lung buds
Then lobar buds
47
At five weeks in the embryonic stage; how many lobar buds on each side
3 on right, 2 on left
48
Lung buds also called,
Respiratory diverticulum
49
The cells lining the lung buds are derived from where
The endoderm
50
The blood vessels and connective tissues surrounding the lungs are derived from where
The mesoderm
51
What happens in the pseudoglandular stage
Rapid branching of the airways
52
Eventually how many segmental bronchi are formed in the pseudoglandular stage?
16-25 primitive segmental bronchi are formed
53
Which specialised cells appear in the airways in the pseudoglandular stage?
Cilia and mucous glands in the airways
54
What develops in the Canalicular stage? (Gas exchange units)
Terminal bronchioles
Alveolar sacs
Capillary blood vessels
55
Which special cells appear in the Canalicular stage?
Type 1 and type 2 celks
56
Type 1 vs type 2 cells
Type 1: thin membrane, allow gas exchange
Type 2: produce and store surfactant
57
Why can babies be born late stage of the canal is half stage, which is 16-26 weeks?
Type 1 and 2 have developed. Limit of viability
With intensive care support
58
What is the exact week for limit of viability
24 weeks onward
59
What happens in the Saccular stage (24-38 weeks)
Alveoli grow with thinner walls, more surfactant produced, bronchioles elongate
60
What happens to interstitial tissue between alveolar sacs
It reduces
61
What stage can sustain breathing without support
Final stage
‘Alveolar’
36 weeks - term and beyond
62
Alveolar sacs become what after birth
Alveoli
63
20-60 million air sacs at birth?
Yea
64
How many air sacs at 3-8 years?
200-300 million
65
How do we discover congenital abnormalities? (2)
Antenatal screening: such as ultrasound and MRI
Newborn: tachypnoea, respiratory distress, feeding issues
66
Older children may present how, if with congenital abnormalities? (4)
(Childhood)
Stridor/wheeze
Recurrent pneumonia
Cough
Feeding issues
67
Laryngomalacia is a congenital abnormality that presents how?
With stridor, worse with feeding or when upset/excited
68
What is laryngomalacia?
Floppiness, collapse of larynx
69
What’s tracheomalacia?
Abnormal collapse of tracheal walls
70
Tracheomalacia presents how? (4)
Barking cough
Recurrent croup
Breathless on exertion
Stridor/wheeze
71
Management of tracheomalacia?
Includes physio and antibiotics when unwell
Natural history, resolution with time
72
What’s the congenital abnormality tracheo-oesphageal fistula?
Abnormal connection between trachea and oesophagus
(Meant to just lie against each other)
73
When is tracheo-oesphageal fistula diagnosed?
Antenatally or postnatally- can be either
74
How does tracheo-oesphageal fistula present?
Choking
Colour change
Cough when feeding
75
Treatment of tracheo-oesphageal fistula?
Surgical repair
76
Leak and reflux, tracheomalacia, strictures are all complications found where
tracheo-oesphageal fistula
77
What’s CPAM? (Congenital pulmonary airway malformation)
Congenital pulmonary airway malformation
Is abnormal non-functioning lung tissue
78
When is CPAM usually detected?
80% of the time it’s detected antenatally
79
Would CPAM *need* surgical repair, or could it resolve spontaneously in utero?
Yea
80
If CPAM is asymptomatic, what then?
Conservative management
Surgical intervention may be required
81
Congenital diaphragmatic hernia is mostly diagnosed when
Antenatally
82
Congenital diaphragmatic hernia is what management?
Surgical repair
83
What happens after first breath?
Lungs inflate and fluid in lungs is absorbed
84
Transient Tachypnoea of the newborn can develop and is associated with what?
C section
85
Transient tachypnoea of the newborn can improve how quickly?
Improves within 1-2 days
86
What’s the treatment for IRDS?
Antenatal steroids
Surfactant replacement
Appropriate ventilation
87
What is chronic lung disease associated with? And what’s required?
Prematurity, ongoing oxygen requirement at term
88
What’s remodelling?
Alteration of airway structure following external influence
89
3 reasons why remodelling might occur?
Environmental exposures
Chronic diseases of childhood
Infection
90
How might remodelling lead to abnormalities?
Due to interference of inter-cellular signalling
91
Remodelling is never seen in asthma, only chronic lung disease of prematurity
False
Remodelling is also seen in asthma
92
How come remodelling is seen in asthma? (4)
Chronic inflammation, therefore:
Increased bronchial responsiveness
Increase mucus secretion
Airway oedema
Airway narrowing
93
Lung function deficits that are established by school age, May track into adult life? And increase risk of what?
Yes
Increase risk of adult lung obstructive diseases, such as COPD
94
What is this describing: ‘200 + diseases causing thickening of the interstitium, and can result in pulmonary fibrosis
ILD
95
What is a typical presentation of idiopathic pulmonary fibrosis?
Chronic breathlessness and cough
Typically 60-70 years old, commoner in men
Clubbed and crackles
96
Median survival of idiopathic pulmonary fibrosis?
3 years
97
Treatment options for idiopathic pulmonary fibrosis?
Oral anti-fibrotic - pirfenidone, nintedanib, palliative care
Surgical option: transplant
98
What type of genetic disorder is cystic fibrosis?
An autosomal recessive disorder
(Of the CFTR gene, on chromosome 7)
99
Both father and mother need to have the CFTR gene for CF to happen
Yah
100
What’s CFTR?
A channel that pumps chloride ions into secretions
101
In newborns with CF, why is lots of extra mucus bad
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
What is meconium ileus?
Meconium- first stool- gets thick and sticky… therefore may get stuck in intestines and not come out ,
103
In early childhood, what’s the most prominent affect of CF? And why
Pancreatic insufficiency
Thick secretions block the pancreatic duct
So not a lot of digestive enzymes make it to the intestines
104
Affect of pancreatic insufficiency, where there are no pancreatic enzymes in the intestines?
No proteins or fat is absorbed
Therefore poor weight gain, and failure to thrive
105
What steatorrhea, and why in CF
If pancreatic insufficiency, fat and proteins not absorbed, so we have fat containing stools
106
Why might the pancreas be damaged?
Because backed up pancreatic enzymes attack the pancreas
(Maybe inflammation and therefore acute pancreatitis)
And therefore chronic pancreatitis
107
Why is cystic fibrosis called cystic fibrosis
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
Why diabetes in CF?
Destruction of pancreatic tissue = compromise endocrine function of the pancreas…Causing insulin-dependant diabetes
109
When do lung problems for Cf crop up
Usually later in childhood
110
In CF what’s wrong with cilia
Mycolciliary ladder are defective cause thick, so bacteria builds,
Therefore
Symptoms like cough and fever
111
CXR issue that prompts
Increased bacterial load = CF exacerbation,
So prompts a round of antibiotics
112
Example of CF exacerbation?
Pneumonia
113
Staphylococcus aureus could never be an issue in CF
Wrong
114
How get bronchiectasis in CF
Chronic bacterial infection and inflammation
115
What is bronchiectasis?
Airway wall damage, causing permanent dilation of the bronchi
Possibly haemoptysis
116
Why respiratory failure in CF? (And therefore death)
Repeated CF exacerbations
117
Digital clubbing might occur in what
CF
118
Infertility in CF might only occur in women
No also men
119
What are nasal polyps
Tissue growths in the nose that might occur in CF
120
What’s ABPA that might occur in CF?
Allergic bronchopulmonary aspergillosus
Which is a hypersensitivity reaction to the fungus aspergillosis fumigatus, which can live in a sinus or lung cavity
121
Diagnosis for CF- to confirm
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
Treatment for CF, nutrition and weight gain (3)
Fat soluble vitamina
Replacement pancreatic enzymes
Extra calories
123
What’s the CF pulmonary treatment?
Chest physiotherapy- banging on chest basically
Inhalers
124
What CF medications?
Meds like n acetylcysteine that cleaves bonds in mucus glycoproteins, or cuts up nucleus acid in mucus to thin it out
125
What to monitor disease in CF
Pulmonary function test
126
Ultimate treatment in CF
Lung transplant
127
Why personalised treatments
To target specific CFTR mutation types
128
What is a lung abscess?
A collection of pus surrounded by granulation tissue?
129
Why do lung abscesses occur? (5)
Aspiration (often cause of pneumonia)
(Maybe drunk, or tooth, or child, or epilepsy seizure = mistake)
Infection causes necrosis
130
What tends to happens to lung abscesses?
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
What’s empyema
Pus in pleural space
132
With pneumonic patient… patient suddenly experiences sudden onset of severe chest pain, which is pleuritic in nature = what
Onset of pyogenic empyema
133
If leakage of pus is very localised, would still be considered a lung abscess vs if spread through whole pleural cavity, it’s called:
Empyema (or empyema thoracis)
134
What might happen post operative, following an infection that progresses into the chest
Empyema
135
Following infection, with fibropurulent covering, and loads of pus, stops kings doing what
Expanding
136
What’s decortication
Surgical removal of the surface layer, membrane, or fibrous cover of an organ
137
Why would decortication happen
When the lung is covered by a thick, I elastic pleural peel restricting lung expansion
138
What’s a pleurectomy
Peeling the parietal pleura off the chest wall
139
What are thymic tumours linked to
Myasthenia gravis
140
Are thymomas always malignant?
Yes
141
Thymic carcinoma is the worst thymic tunour
Yes
142
Why are thymic tumours so bad?
They tend to invade locally into surrounding structures, such as the heart, great vessels, aortic arch
143
When could you operate on a thymic tumour, when they invade where?
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
Why might thymic tumours have adjuvant chemotherapy, or radiotherapy after surgery?
They have a very close resection margin
We follow them for 5 years
145
Are thymomas responsive to chemo and radiotherapy?
Yes
146
Prognosis for thymomas vs carcinoid tumours?
Thymomas have okay prognosis
Carcinoid tumours are frequently not curable by surgery, and tend to reoccur
147
Is tracheal surgery common?
Not at all
148
When might you do tracheal surgery?
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
Primary or secondary pneumothorax?
Primary = no underlying, might just be one portion e.g. apex
Secondary = widespread pathology throughout the lungs eg COPD or pulmonary fibrosis
150
Pneumothoraxes are often secondary to what (2)
COPD
Pulmonary fibrosis
151
Would you usually operate on a secondary pneumothorax
Nah
But yea for primary
152
Pneumothorax often results in what
Lung collapse
153
Tension pneumothorax is often associated with what
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
How many of those with a haemopneumothorax, will the bleeding just stop?
About 50%
155
For a haemopneumothorax where it just continues to bleed?
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
What’s bulbous lung disease?
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
Bullae typically occur in which people
Smokers
158
People with bullae can’t wait
Fly
Could double in size, cause a pneumothorax to develop, or cause tearing of the pulmonary veins around the wall of the bulla
159
A pulmonary embolism is a type of what
Pulmonary vascular disease
160
Pulmonary hypertension is a type of what disease
Pulmonary vascular disease
161
Is cancer a risk factor for venous thromboembolism?
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
Why pregnancy risk for venous thromboembolism
Pregnant =
Clotting factors
Fetus pressing on veins
163
Thrombophilia predisposes you to what?
Thrombosis
164
3 groups of symptoms for pulmonary embolism depending on the size?
Pleuritic chest pain, cough and haemoptysis
Isolated acute dyspnoea
Syncope or cardiac arrest if massive PE
165
Signs of pulmonary embolism based on severity:
1. Pyrexia, pleural rub, stony dullness to percussion at base (pleural effusion)
2. Tachycardia, tachypnoea, hypoxia
3. Tachycardia, hypotension, tachypnoea, hypoxia
166
Why is transient pyrexia a sign of pulmonary embolism?
Well part of the lung tissue has infarcted
167
What sound might you hear with a pulmonary embolism?
A pleural rub
168
Do you always get a pleural effusion with pulmonary embolism?
No
169
If you suspect a pulmonary embolism, what is it important to do?
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
For the wells score, what number suggests suggest PE is unlikely to likely:
0-4 points is unlikely
>4 points is likely
171
Would you do a fbc for PE?
Yah
172
Would you do CXR for pulmonary embolism?
Yh
Though CXR often looks normal, although sometimes you can have subtle abnormalities
173
In the acute stage, would the CXR of a PE more likely to look normal or not?
CXR looks normal often at acute stage
174
What would an ECG show in a pulmonary embolism?
Sinus tachycardia
175
What’s a d dimer- low?
If low or negative, pulmonary embolism very unlikely
176
If you’ve got a low wells score and a negative d-dimer?
You could reasonably discount pulmonary embolism as a diagnosis
177
Would you ever do a CT pulmonary angiogram for PE?
Yeah
178
What would you see in V/Q scan for pulmonary embolism?
Absence of perfusion is due to pulmonary embolism
179
Treatment of hypoxic patient in PE?
Oxygen
180
If PE is strongly suspected, what treatment?
Low molecular weight heparin in a therapeutic dose- even before CT scan
181
What’s heparin
Anticoag
182
If a massive pulmonary embolism, patient is shocked, what treatment might you give?
Thrombolysis
183
Would you give both thrombolysis and low molecular weight heparin?
Ideally not
184
Ideally low molecular weight heparin for pulmonary embolism, or thrombolysis?
Low
185
If massive PE then what
Def thrombolysis
186
What does thrombolysis do
Dissolve the clot essentially
187
What’s a pulmonary embelectomy
It’s a surgical procedure
188
Idiopathic pulmonary arterial hypertension typically presents in which people?
Young adults
189
Pulmonary hypertension eventually leads to what heart failure?
Right
190
Would pulmonary hypertension ever be secondary to left sided heart disease
Yeah
Eg mitral stenosis
191
Could you get pulmonary hypotension secondary to any chronic respiratory disease? Which ones for example?
Yea
Eg severe COPD, sleep apnoea, interstitial lung disease,
Shunt you see
192
What could repeated pulmonary embolisms lead to?
Pulmonary hypertension
193
4 symptoms of pulmonary hypertension?
Exertions dyspnoea
Chest tightness
Exertion all presyncope or syncope
Haemoptysis
194
Signs of pulmonary hypertension
Elevated JVP
Right ventricular heave
Loud pulmonary secondary heart sound
Hepatomegaly
Ankle oedema
195
Why elevated JVP in pulmonary hypertension?
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
Why might you feel a ventricular heave in pulmonary hypertension?
Maybe due to failure of the right ventricle
197
Investigations for pulmonary hypertension.
ECG
Lung function test
CXR
Echocardiography
V/Q scan
198
What’s the most important pulmonary hypertension investigation probs
Echocardiography
199
What’s right heart catheterisation (might do to confirm pulmonary hypertension)
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
What’s Doppler test for p hypertension
Often tricuspid valve leaks a bit
So can use Doppler physiology to measure the velocity of that leak
201
General treatment of pulmonary hypertension?
Treat underlying condition
Oxygen
Anticoagulant
Diuretics
202
When might you use calcium channel antagonists?
If positive vasodilator trial, for pulmonary hypertension
203
What’s the positive vasodilator test for calcium channel antagonists
See if patient will respond to calcium channel antagonists
204
What’s narcolepsy?
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
What are the 5 signs of narcolepsy?
Excessive daytime sleepiness
Sudden loss of muscle tone/ cataplexy
Sleep paralysis
Hallucinations
Changes in REM sleep
206
What’s cataplexy
Temporary loss of muscle control resulting in weakness and possible collapse, often in response to emotions such as laughter and anger
207
PaCO2 May be low in type 1 respiratory failure
True
208
Which type of respiratory failure is most common?
Type 1
209
Type 1 resp failure results from failure of what?
Failure of oxygenation only
Problem with 1 gas only
(Type 1 = problem with 1 gas, type 2 = problem with 2 gases)
210
In a normal lung, the interstitium is made up of fibrous tissue between the basement membranes of the alveolar epithelium and the capillaries
False
In a healthy lung, the alveolar wall and the surrounding capillaries are in direct contact, to allow efficient gas diffusion and exchange
211
Why haemoptysis in CF
(Often) caused by destruction of the bronchial walls through the CF disease process
212
Narcolepsy is associated with delayed onset of REM sleep
False
It is associated with rapid onset of REM sleep, and hallucinations at the time of falling asleep and/or waking
213
Hypoxaemia due to a large shunt does not respond well to supplementary oxygen
Increasing the oxygen concentration in the alveoli will therefore have no impact on the oxygenation of the blood
214
Congenital pulmonary airway malformation can occasionally be associated with risk of malignant change
True
215
Epworth sleepiness score of what or more is considered abnormal?
A score of 11 or more is abnormal
216
Idiopathic pulmonary hypertension is common
False
Very rare
217
What does an opiate overdose do?
Suppress respiratory drive, and cause type 2 respiratory failure by causing alveolar hypoventilation
218
What does diffuse alveolar damage occur from?
Results from acute lung injury/inflammation
Incl. chemical injury, respiratory viruses incl covid, drug effects, major trauma
219
Gas exchange units form when during development
Canalicular
