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Phase 3 > Week 8 > Flashcards

Week 8 Flashcards

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1
Q

What is the definition of COPD?

A

airlflow obstruction which is usually progressive, not fully reversible and does not change markedly over several months
the disease is commonly caused by smoking

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2
Q

Describe the effects of cigarette smoking on the lungs

A

cilial motility is reduced
airway inflammation
mucous hypertrophy and hypertrophy of goblet cells
increased protease activity, anti-proteases inhibited
oxidative stress
squamous metaplasia - higher risk of lung cancer

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3
Q

Describe alpha 1 anti-trypin deficiency

A

present in 1-3% COPD patients
serine proteinase inhibitor
M alleles normal variant
SS and ZZ homozygous have clinical disease
unable to counterbalance destructive enzymes in the lung
non smokers get emphysema in 30s-40s
smokers get it mu earlier

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4
Q

What are the 2 main aspects of COPD?

A

chronic bronchitis

emphysema

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5
Q

Describe chronic bronchitis

A

the production of sputum on most days for at leaser 3 months in at least 2 years

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6
Q

Describe emphysema

A

abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles

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7
Q

Describe the pathophysiology of chronic bronchitis

A 
infiltration with neutrophils and CD8+ lymphocytes
squamous metaplasia
loss of interstitial support
increased epithelial mucous cells
mucous gland hyperplasai
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8
Q

Describe bronchiolitis

A

small airways disease
may be an early feature of COPD
narrowing of bronchioles due to mucous plugging, inflammation and fibrosis

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9
Q

What cells are principally involved in COPD inflammation?

A

macrophages
CD8+ and CD4+ lymphocytes
neutrophils

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10
Q

What inflammatory mediators are involved in COPD inflammation?

A

TNF, IL-8 and other chemokines
neutrophil elastase, proteinase 3, cathepsin G
elastase and MMPs (form macrophages)
reactive oxygen species

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11
Q

What are the 2 main types of emphysema?

A

centri macinar and pan acinar

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12
Q

Describe centri-acinar emphysema

A

damage around the respiratory bronchioles

more in upper lobes

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13
Q

Describe pan -acinar emphysema

A

uniformly enlarged from the level of terminal bronchiole distally
can get large bull
associated with alpha 1 anti-trypsin deficiency

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14
Q

What are the mechanisms of airflow obstruction in COPD

A

loss of elasticity and alveolar attachments due to emphysema - airways collapse on expiration
causes air trapping and hyperinflation - increased work of breathing, breathlessness
goblet cell metaplasia and mucous plugging of lumen
inflammation of airway wall
thickening of bronchiolar wall - smooth muscle hypertrophy and peribronchial fibrosis

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15
Q

What are the changes in a chest X-ray in COPD?

A 
hyperinflation of the lungs
trapping of air in peripheries
flattening of diaphragm 
heart appears small and thin
lungs look blacker - loss of blood vessels
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16
Q

When should the diagnosis of COPD be considered?

A 
those who are over 35, smokers or ex-smokers, with any of:
exertional breathlessness
chronic cough
regular sputum production 
frequent winter bronchitis 
wheeze
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17
Q

Describe spirometry of COPD

A 
FEV1/FVC ration <70%
FEV1 at each stage
1(mild) - 80%
2(moderate) - 50-79%
3(severe) - 30-49%
4(very severe) - <30%
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18
Q

What are the treatments of COPD?

A 
inhaled bronchodilators 
inhaled corticosteroids
oral theophylline
mucolytics - carbocysteine 
nebulised therapy
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19
Q

What types of inhaled bronchodilators are there?

A

short acting - salbutamol

long acting - salmeterol, tiotropium

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20
Q

What types of inhaled corticosteroids are there?

A

budesonide and fluticasone - combination inhalers

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21
Q

Describe a blue bloater

A 
low respiratory drive
type 2 respiratory failure
low O2, high CO2
cyanosis
warm peripheries
bounding pulse
flapping tremor
confusion, drowsiness
right heart failure
oedema, raised JVP
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22
Q

Describe a pink puffer

A 
high respiratory drive
type 1 respiratory drive
O2 and CO2 down
desaturates on exercise
pursed lip breathing
use accessory muscles 
wheeze 
indrawing of intercostals
tachypnoea
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23
Q

What are involved in asthmatic airway inflammation?

A

CD4+
T lymphocytes
eosinophils

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24
Q

What is the primary derangement in metabolic acidosis and what is the compensation?

A

Low HCO3

low CO2

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25
What is the primary derangement in metabolic alkalosis and what is the compensation?
high HCO3 | high CO2
26
What is the primary derangement in respiratory acidosis and what is the compensation?
high CO2 | may be high HCO3
27
What is the primary derangement in respiratory alkalosis and what is the compensation?
low CO2 | may be low HCO3
28
What is compensation?
attempt to restore the correct acid-base balance
29
What are the main buffers in acid-base balance?
haemoglobin plasma proteins bicarbonate phosphate
30
When should you suspect a mixed acid-base disorder?
inadequate or extreme compensation CO2 and HCO3 become abnormal in the opposite direction the pH is normal but CO2 and HCO3 is abnormal
31
What does it mean if the PCO2 is high and the HCO3 is low?
respiratory and metabolic acidosis
32
What does it mean id PCO2 is low and HCO3 is high?
respiratory and metabolic alkalosis
33
What is the normal range for H+?
35-45
34
What is the normal range for PCO2?
4.5-5.6
35
What is the normal range for PO2?
12-15
36
How is the anion gap calculated?
sodium - (chloride +bicarb)
37
What is the normal anion gap?
8-16
38
What are the causes of metabolic acidosis with raised anion gap?
renal failure diabetic or other ketoacidosis lactic acidosis toxins - salicylate, methanol
39
What are the causes of metabolic acidosis with normal anion gap?
renal tubular acidosis diarrhoea carbonic anhydrase inhibitors ureteric diversion
40
How is the osmolal gap calculated?
measured osmolality-calculated osmolality
41
How is osmolality calculated?
2X(sodium and potassium) + urea +glucose (all in mol/L
42
What is the normal OG?
<10mOsm/kg
43
Describe non-invasive ventilation in COPD
provides positive pressure to the airways to support breathing recommended as the first line intervention in addition to usual medical care in COPD exacerbations with persistent hypercapnia respiratory failure considered if there is a respiratory acidosis present or persists despite maximum medical therapy
44
What is cor pulmonale?
right heart failure secondary to lung disease | salt and water retention leading to peripheral oedema
45
What are the signs of cor pulmonale?
``` peripheral oedema raise JVP systolic parasternal heave loud pulmonary second heart sound pulmonary hypertension and right ventricular hypertrophy may develop ```
46
What is the treatment of cor pulmonale?
diuretics
47
Why do we measure lung function?
evaluation of the breathless patient lung cancer - fitness for treatment pre-operative assessment disease progression and treatment response monitoring of drug treatment toxic to the lungs pulmonary complications of systemic disease
48
What is spirometry?
forced expiratory manoeuvre from total lung capacity followed by flu inspiration
49
What are the pitfall of spirometry?
appropriately trained technician effort and technique dependent patient frailty pain, patient too unwell
50
Describe obstructive lung disease
generally asthma or COPD | FEV1/FVC ratio <70%
51
Describe reversibility testing in obstructive lung disease
nebulised or inhaled salbutamol given spirometry before and 15 min after salbutamol 15% and 400mL reversibility of FEV1 suggestive of asthma
52
What other investigations can be used in asthma?
PEFR testing - diurnal variation and variation over time bronchial provocation spirometry before and after trial of inhaled/ oral corticosteroid
53
Describe restrictive lung disease
FEV1 and FVC reduced | FEV1/FVC ratio >70%
54
What can cause restrictive spirometry?
``` interstitial lung disease kyphoscoliosis/ chest wall abnormality previous pneumonectomy neuromuscular disease obesity poor effort/technique ```
55
Describe transfer factor
single breath of very small concentration of CO high affinity to Hb measure concentration in expired gas to derive uptake upon lungs
56
What is transfer factor affected by?
alveolar surface area pulmonary capillary blood volume haemoglobin concentration ventilation perfusion mismatch
57
What is transfer factor reduced in?
emphysema interstitial lung disease pulmonary vascular disease anaemia (increased in polycytaemia)
58
How can lung volumes be measured?
``` helium dilution (inspire known quantity of inert gas) body plethysmography (respiratory manoeuvres in a seal box lead to changed in air pressure - can derive lung volumes ```
59
What is oximetry?
non-invasive measurement of saturation of Hb by oxygen depends of oxyhemoglobin and deoxyhaemoglobin absorbing infrared differently Does not measure carbon dioxide so no measurement of ventilation false reassurance in a patient on oxygen with normal Sats
60
What are the main causes of hypoxaemia?
hypoventilation ventilation/perfusion mismatch shunt low inspired oxygen
61
Describe VQ mismatch
main cause of hypoxaemia in medical patients read of the lung that are perfused but not well ventilated mixing of blood from poorly ventilated and well ventilated parts of the lung cause hypoxaemia does not fully correct with oxygen administration
62
Describe extra-thoracic disease
``` not susceptible to intra-thoracic pressure for example laryngeal oedema stridor flow-volume loops aspiration to right middle/lower lobe ```
63
What are the clinical consequences of bronchial disease
medium - small airways flaccid walls- not supported by cartilage, expiratory phase narrowing (wheeze) much-ciliary clearance impairment - sputum characteristic flow volume loops
64
What is the clinical definition of asthma?
appropriate symptoms with signs - wheeze, cough, yellow/clear sputum breathlessness, exercise intolerance episodic, triggered, variable - paroxysmal - exercise, cats, chemicals diurnal -nocturnal awakening respond to asthma therapies
65
What is the physiological definition of asthma?
reversible airflow obstruction | airways hyper-responsiveness
66
What cytokines are overproduced in asthmatic airways ?
``` IL5 TSLP IL13 TNFalpha TGFbeta VEGF ```
67
What are the main cells involved in asthma?
mast cells lympohcyes macrophages epithelial cells
68
What airway remodelling can occur in chronic asthma?
angiogenesis epithelial cell damage fibrosis smooth muscle hypertrophy
69
Describe the acute illness of allergic disease in the lung parenchyma
4-6 hours after exposure wheeze, cough, fever, chills, headache, myalgia, malaise fatigue may last several days serum sickness illness
70
What are the clinical consequences of allergic disease in the lung parenchyma?
thickening of septae, filling of the alveolus with fluid loss of O2 - hypoxaemia (normal Co2) airspace shadowing on CXR
71
What can chronic exposure in allergic disease of the lung parenchyma lead to?
fibrosis - interstitial scarring from chronic tissue remodelling - repair pathways emphysema- interstirtial destruction from neutrophilic enzyme release
72
Describe extrinsic allergic alveolitis
acute illness due to type III reaction sub acute days to weeks type IV- t cell mediated reactions chronic disease - fibrosis and emphysema
73
What is the treatment of extrinsic allergic alveoli's?
avoid trigger corticosteroids oxygen supplementation
74
What is obstructive sleep apnoea?
recurrent episodes of partial or complete upper airway obstruction during sleep, intermittent hypoxia and sleep fragmentation
75
What is obstructive sleep apnoea syndrome?
manifests as excessive daytime sleepiness
76
What are the symptoms of obstructive sleep apnoea?
``` snorer witnessed apnoeas unrefreshed sleep daytime somnolence fatigue/low mood/poor concentration ```
77
How is OSA assessed?
``` history - from partner weight BMI BP neck circumference craniofacial appearance tonsils nasal patency ```
78
What is involved in limited polysomnography?
``` 5 channel home study oxygen Sats heart rate flow thoracic and abdominal effort position ```
79
What is involved in full polysomnography?
``` EEG video audio thoracic and abdominal bands position flow oxygen sats limb leads snore ```
80
What are the advantages of full PSG?
correct patient accurate assessment of sleep effiency sleep staging via EEG parasomnic activity - acting out dreams, sleep talking
81
What is apnea?
the cessation or near cessation of airlflow | 4% oxygen desaturation lasting >4secondsa
82
What is hypopnea?
a reduction of airflow to a degree insufficient to meet the criteria for an apnoae
83
What are respiratory effort related arousals?
arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnoea
84
What is the apnoea-hypopnea index?
the number of apnoeas and hypopnoeas per hour
85
What is the oxygen desaturation index?
the number of times per hour that the SpO2 falls atlas 4% from baseline
86
What is the diagnostic criteria for AHI in OSA?
>15 is diagnostic | 5-15 with compatible symptoms
87
What is the treatment of OSAS?
explanation weight loss avoid triggers - alchohol treat underlying conditions - tonsils, hypothyroidism, nasal obstruction
88
What does CPAP do?
splints airway open stops snoring stops sleep fragmentation
89
What can untreated OSAS lead to?
``` hypertension right heart strain cardiovascular disease increased risk of CVA increased accidents at work poor concentration increased road traffic accidents ```
90
Describe OSAS and driving
without daytime somnolence - no need to stop driving inform DVLA is OSAS can hold licence if compliant with treatment and reduced DTS cat 2 licence require ongoing monitoring by DVLA
91
What is a pneumothorax?
air within the pleural cavity
92
What types of pneumothorax are there?
traumatic, iatrogenic, spontaneous
93
What can cause a traumatic pneumothorax?
stabbing | fractured rib
94
What can cause an iatrogenic pneumothorax?
CT guided lung biopsy TBLB pleural aspiration
95
What can cause a spontaneous pneumothorax?
primary - young patient, no underlying lung disease | secondary, underlying disease (COPD, cystic fibrosis)
96
Describe a tension pneumothorax
medical emergency one way valve leads to increased intrapleural pressure venous return impaired, cardiac output and blood pressure fall PEA arrest without intervention
97
What is the immediate management of a tension pneumothorax?
insert venflon 2nd intercostal space mid-clavicular line to relieve pressure
98
What is the pathophysiology of primary pneumothorax?
development of subpleural blebs/bullae at lung apex possible additional diffuse, microscopic emphysema below the surface of the visceral pleura spontaneous rupture leads to tear in visceral pleura air flows from the airways to pleural space elastic lung then collapses
99
Describe the pathophysiology of secondary pneumothorax
inherent weakness in lung tissue increased airway pressure increased lung elasticity patient is generally much more symptomatic management more complex, prognosis less good
100
What are the symptoms and signs of pneumothorax?
``` pleuritic chest pain breathlessness respiratory distress reduced air entry on affected side hyper-resonance to percussion reduced vocal resonance tracheal deviation if tension ```
101
What is the differential diagnosis of pneumothorax?
PTE musculoskeletal pain pleurisy/ pneumonia
102
What are the management options of pneumothorax?
observation (serial CXR) if small or not very symptomatic aspiration intercostal drain with underwater seal
103
What can be done to treat a pneumothorax if a drain fails to work?
VATS (video assisted thoracic surgery) can stable blebs talk pleurodeses pleural abrasion / stripping
104
What are the clinical predisposing risk factors of PE?
``` surgery <12 weeks previously immobilisation >3 days in previous 4 weeks previous DVT/ PTE or family history lower limb fracture pregnancy or postpartum long distance travel oestrogen containing OCP use ```
105
What are the symptoms of PE?
``` pleuritic chest pain dyspnoea cough haemoptysis syncope ```
106
What are the signs of PE?
``` tachypnoea crackles tachycardia fever signs of peripheral DVT ```
107
What are the acute changes in the pathophysiology of PE?
anatomical obstruction of pulmonary vascular bed increased pulmonary vascular resistance right ventricular strain reduced mixed venous oxygen content, right to left shunting through PFO increase in alveolar-arterial gradient. hypoxaemia in large PTE
108
What are the investigations for PE?
``` risk assessment - modified geneva D -dimer arterial blood gases - troponin level ECH echocardiogram radiology - CXR, CT pulmonary angiogram, V/Q scan ```
109
What is expected to be seen in the arterial blood gases in a PE?
usually respiratory alkalosis | hypoxaemia only seen with large PE
110
Why is an echocardiogram used in investigation of PE?
to look for RV strain
111
What is the treatment of massive pulmonary embolism?
unfractionated heparin IV fluid resuscitation thrombolysis with alteplase if fails to improve
112
What is a massive pulmonary embolism?
PE associated with a systolic BP <90 or a drop of systolic BP >40 mmHg in <15 minutes
113
What is the treatment of sub-massive PE?
low molecular weight heparin -dalterparin oral anti-coagulation for 3 months factor Xa inhibitors warfarin
114
What is sarcoidosis?
a multisystem inflammatory disease of unknown ethology that predominantly affects the lungs and intrathoracic lymph nodes. Characterised by non necrotising granulomatous inflammation
115
What can be the presentation of sarcoidosis?
``` fever anorexia fatigue night sweats weight loss dyspnoea cough chest pain haemoptysis ```
116
Describe idiopathic pulmonary fibrosis
``` age >50 M:F 2:1 progressive breathlessness bibasilar crackles, clubbing peripheral interstitial pattern subpleural honeycombing ```
117
What are the symptoms of IPF?
``` breathlessness hacking dry cough fatigue and weakness appetite and weight loss clubbing ```
118
What are the causes of pulmonary fibrosis?
``` occupation and environmental drug induced connective tissue diseases primary disease idiopathic genetics ```
119
What are the occupational and environmental causes of PF?
silicosis asbestosis hypersensitivity pneumonitis
120
What are the drugs which can cause PF?
amioderone nitrofurantoin methotrexate cocaine
121
What are the connective tissue diseases that can cause PF?
lupus RA scleroderma
122
What are the primary diseases that can cause PF?
sarcoidosis | LAM
123
How is PF diagnosed?
HRCT
124
What is hypersensitivity pneumonitis?
immunologically mediated inflammatory reaction in the alveoli and in the respiratory bronchioles T cell mediated response causes - dusts, moulds, foreign proteins (animals), some chemicals
125
What are the symptoms of hypersensitivity pneumonitis?
``` flu like illness cough fever, chills dyspnea chest tightness malaise myalgia chronic - dyspnea in strain, sputum production, fatigue, anorexia, weight loss ```
126
What is the appearance of acute HSP on CXR?
numerous poorly defined small opacities in both lungs sometimes sparing of the apices and bases ground glass opacities fine reticulation zonal distribution
127
Describe the pathology in chronic HSP
bronchocentric pattern foamy macrophages in alveolar spaces chronic interstitial inflammation organising pneumonia
128
What are the risk factors of lung cancer?
``` smoking environmental tobacco smoke ionising radiation - radon air pollution asbestos fibrosing conditions of lung, HPV, hereditary ```
129
Describe the pathogenesis of lung cancer
multi step chronic irrigation/ stimulation of cells by carcinogens increased cell turnover progressive accumulation of genetic abnormalities in molecules involved in cel cycle, signalling and angiogenesis pathways phenotypic changes potentially reversible (but genotypic alterations persist)
130
What are some of the targets of new targeted therapies of lung cancer?
EGFR ALK PD-L1
131
What are the signs and symptoms of lung cancer?
cough haemoptysis chest pain metastases
132
Describe the local spread of lung cancer
mediastinum - SVC obstruction, recurrent laryngeal nerve, phrenic nerve pancoast tumour - brachial plexus, horner's syndrome
133
where do lung cancers typically spread to?
liver, lymph nodes, bone, brain, adrenal gland
134
What are some of the non metazoic effects of lung cancer?
``` ACTH production ADH production PRH production encephalopathy cerebellar degenertion neuropathy myopathy eaton lambert syndrome ```
135
Describe small cell carcinoma
most aggressive form metastasises early and wide good initial treatment response but most relapse
136
What types of non-small cell carcinoma?
sqaumous adenocarcinoma large cell
137
Describe squamous cell carcinoma
major bronchi slow growth - surgery may undergo cavitation may lead to retention pneumonia or collapse
138
Describe adenocarcinoma of the lung
common in females mainly in periphery may produce mucin
139
Describe large cell carcinoma
diagnosis of exclusion | centrally arising
140
What is mesothelioma?
primary pleural tumour | almost always due to asbestos exposure
141
Describe dermatophytes
fungi that cause common infections of skin, nails and hair do not colonise live tissues - only keratinised areas healthy and immunocompromised equally infected ringworm / tinea
142
What is the treatment of dermatophytes?
over the counter products topical administration apart from severe, nail infections terbinafine
143
What are systemic fungal infections?
``` fungal meningitis - cryptococcus neoformans aspergiollosis of lungs aspergillus fumigatus pneumocystic pneumonia pneumocystis jirovec ```
144
Describe cryptococcus neoformans
``` inhaled opportunistic pathogen encapsulated yeast contracted from environment lungs / meningitis 2 weeks of amphotericin B for meningitis fluconazole or flucysosine (non CNS) ```
145
Describe aspergillus fumigatus
allergic bronchopulmonary aspergillosis invasive pulmonary aspergillosis aspergilloma
146
Describe pneumocystis jiroveci
common environmental fungus pneumonia - fever, cough, SOB treatment and prophylaxis - trimethoprim-sulfamethoxazole
147
Describe imidazole, triazole and thiazole antifungals
``` largest class of anti fungal agents many applications multiple types of drugs ```
148
What is the mechanism of action of azole drugs?
inhibitors of 14-methylsterol alpha demethylase which produces ergosterol essential component of fungal plasma membrane does not occur in plant or animal cells
149
Describe the action of amphotericin B
``` exploits ergosterol/cholesterol difference not an enzyme inhibits exploits the presence of ergosterol forms pore in fungal membranes leakage of intracellular cations cell death ```
150
How is a life threatening acute exacerbation of asthma treated?
``` high flow oxygen nebulised bronchodilators (500mg salbutamol, 500mcg ipatropium bromide) oral prednisalone 40mg oral doxycycline 200mg IV magnesium 2g Discussion with ITU consider IV aminophylline infusion ```
151
What is the mechanism of action of corticosteroids?
bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes that are activated in asthmatic airways by reversing histone actetylation
152
What are the indications of inhaled corticosteroids
asthma | COPD with recurrent exacerbations
153
What are the side effects of corticosteroids?
diabetes, osteoporosis, hypertension, muscle wasting, peptic ulcer, cataracts, cushings syndrome, adrenal suppression, acute pancreatitis, hyperlipidaemia, increased appetite, salt and water retention , immune suppresion
154
What is the mechanism of action of Beta 2 agonists?
higher specificity for pulmonary beta 2 receptors vs cardia B1 receptros stimulate adenyl cyclase to increase intracellular cAMP - relaxation of bronchial smooth muscle
155
What are the indications for b2 agonists?
asthma | COPD
156
What are the side effects of B2 agonists?
``` tremor hypokalaemia hypergylcaemia hypomagnasmaemia flushing tachycardia arrhythmias headache muscle cramps ```
157
What is the mechanism of action of anti-muscarinics?
inhibition of cholinergic M1 and M3 receptor in lung - reduction in cGMP and inhibition of parasympathetic mediated broncoconstriction
158
What are the side effects of anti-muscarinics?
blurred vision, dry mouth, urinary retention, nausea, constpiation, nebulised ipatropium may precipitate acute angle closure glaucoma
159
What is the mechanism of action of methylxanthines?
non-selective inhibition of phosphodiesterase - increased cellular cAMP, bronchial smooth muscle relaxation improved mucocilliary clearance and anti-inflammatory effect
160
What are the indications for methylxanthines?
Adjunct to inhaled therapies in asthma / IV infusion in severe exacerbations
161
What are the side effects of methylxanthines?
GI upset, tachycardia, headache , insomnia, hypokalaemia
162
Describe leyukotrine receptro antagonists
bind with high affinity to cysteinyl leukotriene receptor, inhibiting the action of LTDA in smooth muscle cells of the airway and airway macrophages - reduced oedema and smooth muscle contraction
163
Describe omalizumab
monoclonal anti-Ig£ antibody severe persistent allergic asthma subcut injection every 4 weeks
164
Describe mepolizumab
``` anti-IL5 monoclonal antibody reduces circulating eosinophils severe refractory eosinophilic asthma sub cut injection every 4 weeks headaches commonly reported ```
165
Give examples of other drugs used in COPD
roflumilast -reduced inflammation azithromyicin - anti-inflammatory effects carbocysteine - reduced sputum viscosity

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