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Phase 3 > Week 8 > Flashcards

Week 8 Flashcards

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
Q

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

A

high HCO3

high CO2

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26
Q

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

A

high CO2

may be high HCO3

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27
Q

What is the primary derangement in respiratory alkalosis and what is the compensation?

A

low CO2

may be low HCO3

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28
Q

What is compensation?

A

attempt to restore the correct acid-base balance

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29
Q

What are the main buffers in acid-base balance?

A

haemoglobin
plasma proteins
bicarbonate
phosphate

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30
Q

When should you suspect a mixed acid-base disorder?

A

inadequate or extreme compensation
CO2 and HCO3 become abnormal in the opposite direction
the pH is normal but CO2 and HCO3 is abnormal

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31
Q

What does it mean if the PCO2 is high and the HCO3 is low?

A

respiratory and metabolic acidosis

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32
Q

What does it mean id PCO2 is low and HCO3 is high?

A

respiratory and metabolic alkalosis

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33
Q

What is the normal range for H+?

A

35-45

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34
Q

What is the normal range for PCO2?

A

4.5-5.6

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35
Q

What is the normal range for PO2?

A

12-15

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36
Q

How is the anion gap calculated?

A

sodium - (chloride +bicarb)

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37
Q

What is the normal anion gap?

A

8-16

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38
Q

What are the causes of metabolic acidosis with raised anion gap?

A

renal failure
diabetic or other ketoacidosis
lactic acidosis
toxins - salicylate, methanol

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39
Q

What are the causes of metabolic acidosis with normal anion gap?

A

renal tubular acidosis
diarrhoea
carbonic anhydrase inhibitors
ureteric diversion

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40
Q

How is the osmolal gap calculated?

A

measured osmolality-calculated osmolality

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41
Q

How is osmolality calculated?

A

2X(sodium and potassium) + urea +glucose (all in mol/L

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42
Q

What is the normal OG?

A

<10mOsm/kg

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43
Q

Describe non-invasive ventilation in COPD

A

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

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44
Q

What is cor pulmonale?

A

right heart failure secondary to lung disease

salt and water retention leading to peripheral oedema

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45
Q

What are the signs of cor pulmonale?

A 
peripheral oedema
raise JVP
systolic parasternal heave
loud pulmonary second heart sound
pulmonary hypertension and right ventricular hypertrophy may develop
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46
Q

What is the treatment of cor pulmonale?

A

diuretics

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47
Q

Why do we measure lung function?

A

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

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48
Q

What is spirometry?

A

forced expiratory manoeuvre from total lung capacity followed by flu inspiration

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49
Q

What are the pitfall of spirometry?

A

appropriately trained technician
effort and technique dependent
patient frailty
pain, patient too unwell

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50
Q

Describe obstructive lung disease

A

generally asthma or COPD

FEV1/FVC ratio <70%

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51
Q

Describe reversibility testing in obstructive lung disease

A

nebulised or inhaled salbutamol given
spirometry before and 15 min after salbutamol
15% and 400mL reversibility of FEV1 suggestive of asthma

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52
Q

What other investigations can be used in asthma?

A

PEFR testing - diurnal variation and variation over time
bronchial provocation
spirometry before and after trial of inhaled/ oral corticosteroid

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53
Q

Describe restrictive lung disease

A

FEV1 and FVC reduced

FEV1/FVC ratio >70%

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54
Q

What can cause restrictive spirometry?

A 
interstitial lung disease
kyphoscoliosis/ chest wall abnormality
previous pneumonectomy
neuromuscular disease
obesity
poor effort/technique
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55
Q

Describe transfer factor

A

single breath of very small concentration of CO
high affinity to Hb
measure concentration in expired gas to derive uptake upon lungs

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56
Q

What is transfer factor affected by?

A

alveolar surface area
pulmonary capillary blood volume
haemoglobin concentration
ventilation perfusion mismatch

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57
Q

What is transfer factor reduced in?

A

emphysema
interstitial lung disease
pulmonary vascular disease
anaemia (increased in polycytaemia)

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58
Q

How can lung volumes be measured?

A 
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
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59
Q

What is oximetry?

A

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

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60
Q

What are the main causes of hypoxaemia?

A

hypoventilation
ventilation/perfusion mismatch
shunt
low inspired oxygen

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61
Q

Describe VQ mismatch

A

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

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62
Q

Describe extra-thoracic disease

A 
not susceptible to intra-thoracic pressure
for example laryngeal oedema
stridor
flow-volume loops
aspiration to right middle/lower lobe
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63
Q

What are the clinical consequences of bronchial disease

A

medium - small airways flaccid walls- not supported by cartilage, expiratory phase narrowing (wheeze)
much-ciliary clearance impairment - sputum
characteristic flow volume loops

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64
Q

What is the clinical definition of asthma?

A

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

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65
Q

What is the physiological definition of asthma?

A

reversible airflow obstruction

airways hyper-responsiveness

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66
Q

What cytokines are overproduced in asthmatic airways ?

A 
IL5
TSLP
IL13
TNFalpha
TGFbeta
VEGF
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67
Q

What are the main cells involved in asthma?

A

mast cells
lympohcyes
macrophages
epithelial cells

68
Q

What airway remodelling can occur in chronic asthma?

A

angiogenesis
epithelial cell damage
fibrosis
smooth muscle hypertrophy

69
Q

Describe the acute illness of allergic disease in the lung parenchyma

A

4-6 hours after exposure
wheeze, cough, fever, chills, headache, myalgia, malaise fatigue
may last several days
serum sickness illness

70
Q

What are the clinical consequences of allergic disease in the lung parenchyma?

A

thickening of septae, filling of the alveolus with fluid
loss of O2 - hypoxaemia (normal Co2)
airspace shadowing on CXR

71
Q

What can chronic exposure in allergic disease of the lung parenchyma lead to?

A

fibrosis - interstitial scarring from chronic tissue remodelling - repair pathways
emphysema- interstirtial destruction from neutrophilic enzyme release

72
Q

Describe extrinsic allergic alveolitis

A

acute illness due to type III reaction
sub acute days to weeks
type IV- t cell mediated reactions
chronic disease - fibrosis and emphysema

73
Q

What is the treatment of extrinsic allergic alveoli’s?

A

avoid trigger
corticosteroids
oxygen supplementation

74
Q

What is obstructive sleep apnoea?

A

recurrent episodes of partial or complete upper airway obstruction during sleep, intermittent hypoxia and sleep fragmentation

75
Q

What is obstructive sleep apnoea syndrome?

A

manifests as excessive daytime sleepiness

76
Q

What are the symptoms of obstructive sleep apnoea?

A 
snorer
witnessed apnoeas
unrefreshed sleep
daytime somnolence
fatigue/low mood/poor concentration
77
Q

How is OSA assessed?

A 
history - from partner
weight
BMI
BP 
neck circumference 
craniofacial appearance 
tonsils 
nasal patency
78
Q

What is involved in limited polysomnography?

A 
5 channel home study 
oxygen Sats
heart rate
flow
thoracic and abdominal effort
position
79
Q

What is involved in full polysomnography?

A 
EEG
video
audio
thoracic and abdominal bands
position 
flow
oxygen sats
limb leads 
snore
80
Q

What are the advantages of full PSG?

A

correct patient
accurate assessment of sleep effiency
sleep staging via EEG
parasomnic activity - acting out dreams, sleep talking

81
Q

What is apnea?

A

the cessation or near cessation of airlflow

4% oxygen desaturation lasting >4secondsa

82
Q

What is hypopnea?

A

a reduction of airflow to a degree insufficient to meet the criteria for an apnoae

83
Q

What are respiratory effort related arousals?

A

arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnoea

84
Q

What is the apnoea-hypopnea index?

A

the number of apnoeas and hypopnoeas per hour

85
Q

What is the oxygen desaturation index?

A

the number of times per hour that the SpO2 falls atlas 4% from baseline

86
Q

What is the diagnostic criteria for AHI in OSA?

A

> 15 is diagnostic

5-15 with compatible symptoms

87
Q

What is the treatment of OSAS?

A

explanation
weight loss
avoid triggers - alchohol
treat underlying conditions - tonsils, hypothyroidism, nasal obstruction

88
Q

What does CPAP do?

A

splints airway open
stops snoring
stops sleep fragmentation

89
Q

What can untreated OSAS lead to?

A 
hypertension
right heart strain
cardiovascular disease
increased risk of CVA
increased accidents at work
poor concentration
increased road traffic accidents
90
Q

Describe OSAS and driving

A

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
Q

What is a pneumothorax?

A

air within the pleural cavity

92
Q

What types of pneumothorax are there?

A

traumatic, iatrogenic, spontaneous

93
Q

What can cause a traumatic pneumothorax?

A

stabbing

fractured rib

94
Q

What can cause an iatrogenic pneumothorax?

A

CT guided lung biopsy
TBLB
pleural aspiration

95
Q

What can cause a spontaneous pneumothorax?

A

primary - young patient, no underlying lung disease

secondary, underlying disease (COPD, cystic fibrosis)

96
Q

Describe a tension pneumothorax

A

medical emergency
one way valve leads to increased intrapleural pressure
venous return impaired, cardiac output and blood pressure fall
PEA arrest without intervention

97
Q

What is the immediate management of a tension pneumothorax?

A

insert venflon 2nd intercostal space mid-clavicular line to relieve pressure

98
Q

What is the pathophysiology of primary pneumothorax?

A

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
Q

Describe the pathophysiology of secondary pneumothorax

A

inherent weakness in lung tissue
increased airway pressure
increased lung elasticity
patient is generally much more symptomatic
management more complex, prognosis less good

100
Q

What are the symptoms and signs of pneumothorax?

A 
pleuritic chest pain
breathlessness
respiratory distress
reduced air entry on affected side
hyper-resonance to percussion
reduced vocal resonance 
tracheal deviation if tension
101
Q

What is the differential diagnosis of pneumothorax?

A

PTE
musculoskeletal pain
pleurisy/ pneumonia

102
Q

What are the management options of pneumothorax?

A

observation (serial CXR) if small or not very symptomatic
aspiration
intercostal drain with underwater seal

103
Q

What can be done to treat a pneumothorax if a drain fails to work?

A

VATS (video assisted thoracic surgery)
can stable blebs
talk pleurodeses
pleural abrasion / stripping

104
Q

What are the clinical predisposing risk factors of PE?

A 
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
Q

What are the symptoms of PE?

A 
pleuritic chest pain
dyspnoea
cough
haemoptysis
syncope
106
Q

What are the signs of PE?

A 
tachypnoea
crackles
tachycardia
fever
signs of peripheral DVT
107
Q

What are the acute changes in the pathophysiology of PE?

A

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
Q

What are the investigations for PE?

A 
risk assessment - modified geneva 
D -dimer 
arterial blood gases - 
troponin level
ECH 
echocardiogram
radiology - CXR, CT pulmonary angiogram, V/Q scan
109
Q

What is expected to be seen in the arterial blood gases in a PE?

A

usually respiratory alkalosis

hypoxaemia only seen with large PE

110
Q

Why is an echocardiogram used in investigation of PE?

A

to look for RV strain

111
Q

What is the treatment of massive pulmonary embolism?

A

unfractionated heparin IV
fluid resuscitation
thrombolysis with alteplase if fails to improve

112
Q

What is a massive pulmonary embolism?

A

PE associated with a systolic BP <90 or a drop of systolic BP >40 mmHg in <15 minutes

113
Q

What is the treatment of sub-massive PE?

A

low molecular weight heparin -dalterparin
oral anti-coagulation for 3 months
factor Xa inhibitors
warfarin

114
Q

What is sarcoidosis?

A

a multisystem inflammatory disease of unknown ethology that predominantly affects the lungs and intrathoracic lymph nodes. Characterised by non necrotising granulomatous inflammation

115
Q

What can be the presentation of sarcoidosis?

A 
fever
anorexia
fatigue
night sweats
weight loss
dyspnoea
cough
chest pain
haemoptysis
116
Q

Describe idiopathic pulmonary fibrosis

A 
age >50
M:F 2:1
progressive breathlessness
bibasilar crackles, clubbing
peripheral interstitial pattern
subpleural honeycombing
117
Q

What are the symptoms of IPF?

A 
breathlessness
hacking dry cough 
fatigue and weakness
appetite and weight loss 
clubbing
118
Q

What are the causes of pulmonary fibrosis?

A 
occupation and environmental 
drug induced
connective tissue diseases 
primary disease 
idiopathic 
genetics
119
Q

What are the occupational and environmental causes of PF?

A

silicosis
asbestosis
hypersensitivity pneumonitis

120
Q

What are the drugs which can cause PF?

A

amioderone
nitrofurantoin
methotrexate
cocaine

121
Q

What are the connective tissue diseases that can cause PF?

A

lupus
RA
scleroderma

122
Q

What are the primary diseases that can cause PF?

A

sarcoidosis

LAM

123
Q

How is PF diagnosed?

A

HRCT

124
Q

What is hypersensitivity pneumonitis?

A

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
Q

What are the symptoms of hypersensitivity pneumonitis?

A 
flu like illness
cough 
fever, chills
dyspnea 
chest tightness
malaise 
myalgia 
chronic - dyspnea in strain, sputum production, fatigue, anorexia, weight loss
126
Q

What is the appearance of acute HSP on CXR?

A

numerous poorly defined small opacities in both lungs
sometimes sparing of the apices and bases
ground glass opacities
fine reticulation
zonal distribution

127
Q

Describe the pathology in chronic HSP

A

bronchocentric pattern
foamy macrophages in alveolar spaces
chronic interstitial inflammation
organising pneumonia

128
Q

What are the risk factors of lung cancer?

A 
smoking 
environmental tobacco smoke 
ionising radiation - radon
air pollution
asbestos
fibrosing conditions of lung, HPV, hereditary
129
Q

Describe the pathogenesis of lung cancer

A

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
Q

What are some of the targets of new targeted therapies of lung cancer?

A

EGFR
ALK
PD-L1

131
Q

What are the signs and symptoms of lung cancer?

A

cough
haemoptysis
chest pain
metastases

132
Q

Describe the local spread of lung cancer

A

mediastinum - SVC obstruction, recurrent laryngeal nerve, phrenic nerve
pancoast tumour - brachial plexus, horner’s syndrome

133
Q

where do lung cancers typically spread to?

A

liver, lymph nodes, bone, brain, adrenal gland

134
Q

What are some of the non metazoic effects of lung cancer?

A 
ACTH production
ADH production 
PRH production
encephalopathy
cerebellar degenertion
neuropathy
myopathy
eaton lambert syndrome
135
Q

Describe small cell carcinoma

A

most aggressive form
metastasises early and wide
good initial treatment response but most relapse

136
Q

What types of non-small cell carcinoma?

A

sqaumous
adenocarcinoma
large cell

137
Q

Describe squamous cell carcinoma

A

major bronchi
slow growth - surgery
may undergo cavitation
may lead to retention pneumonia or collapse

138
Q

Describe adenocarcinoma of the lung

A

common in females
mainly in periphery
may produce mucin

139
Q

Describe large cell carcinoma

A

diagnosis of exclusion

centrally arising

140
Q

What is mesothelioma?

A

primary pleural tumour

almost always due to asbestos exposure

141
Q

Describe dermatophytes

A

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
Q

What is the treatment of dermatophytes?

A

over the counter products
topical administration apart from severe, nail infections
terbinafine

143
Q

What are systemic fungal infections?

A 
fungal meningitis - cryptococcus neoformans 
aspergiollosis of lungs
aspergillus fumigatus
pneumocystic pneumonia
pneumocystis jirovec
144
Q

Describe cryptococcus neoformans

A 
inhaled opportunistic pathogen
encapsulated yeast
contracted from environment 
lungs / meningitis
2 weeks of amphotericin B for meningitis 
fluconazole or flucysosine (non CNS)
145
Q

Describe aspergillus fumigatus

A

allergic bronchopulmonary aspergillosis
invasive pulmonary aspergillosis
aspergilloma

146
Q

Describe pneumocystis jiroveci

A

common environmental fungus
pneumonia - fever, cough, SOB
treatment and prophylaxis - trimethoprim-sulfamethoxazole

147
Q

Describe imidazole, triazole and thiazole antifungals

A 
largest class of anti fungal agents 
many applications 
multiple types of drugs
148
Q

What is the mechanism of action of azole drugs?

A

inhibitors of 14-methylsterol alpha demethylase which produces ergosterol
essential component of fungal plasma membrane
does not occur in plant or animal cells

149
Q

Describe the action of amphotericin B

A 
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
Q

How is a life threatening acute exacerbation of asthma treated?

A 
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
Q

What is the mechanism of action of corticosteroids?

A

bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes that are activated in asthmatic airways by reversing histone actetylation

152
Q

What are the indications of inhaled corticosteroids

A

asthma

COPD with recurrent exacerbations

153
Q

What are the side effects of corticosteroids?

A

diabetes, osteoporosis, hypertension, muscle wasting, peptic ulcer, cataracts, cushings syndrome, adrenal suppression, acute pancreatitis, hyperlipidaemia, increased appetite, salt and water retention , immune suppresion

154
Q

What is the mechanism of action of Beta 2 agonists?

A

higher specificity for pulmonary beta 2 receptors vs cardia B1 receptros
stimulate adenyl cyclase to increase intracellular cAMP - relaxation of bronchial smooth muscle

155
Q

What are the indications for b2 agonists?

A

asthma

COPD

156
Q

What are the side effects of B2 agonists?

A 
tremor
hypokalaemia
hypergylcaemia
hypomagnasmaemia
flushing 
tachycardia
arrhythmias
headache
muscle cramps
157
Q

What is the mechanism of action of anti-muscarinics?

A

inhibition of cholinergic M1 and M3 receptor in lung - reduction in cGMP and inhibition of parasympathetic mediated broncoconstriction

158
Q

What are the side effects of anti-muscarinics?

A

blurred vision, dry mouth, urinary retention, nausea, constpiation,
nebulised ipatropium may precipitate acute angle closure glaucoma

159
Q

What is the mechanism of action of methylxanthines?

A

non-selective inhibition of phosphodiesterase - increased cellular cAMP, bronchial smooth muscle relaxation
improved mucocilliary clearance and anti-inflammatory effect

160
Q

What are the indications for methylxanthines?

A

Adjunct to inhaled therapies in asthma / IV infusion in severe exacerbations

161
Q

What are the side effects of methylxanthines?

A

GI upset, tachycardia, headache , insomnia, hypokalaemia

162
Q

Describe leyukotrine receptro antagonists

A

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
Q

Describe omalizumab

A

monoclonal anti-Ig£ antibody
severe persistent allergic asthma
subcut injection every 4 weeks

164
Q

Describe mepolizumab

A 
anti-IL5 monoclonal antibody
reduces circulating eosinophils
severe refractory eosinophilic asthma
sub cut injection every 4 weeks
headaches commonly reported
165
Q

Give examples of other drugs used in COPD

A

roflumilast -reduced inflammation
azithromyicin - anti-inflammatory effects
carbocysteine - reduced sputum viscosity

Phase 3 (15 decks)

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