Unit 8 Case 3: COPD Flashcards

1
Q

what is COPD

A

Chronic obstructive pulmonary disease ​

Umbrella term for a group of lung conditions that cause breathing difficulties

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2
Q

2 main conditions involved in COPD

A

emphysema
chronic bronchitis

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3
Q

3 different types of emphysema

A

centriacinar
panacinar
paraseptal

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4
Q

centriacinar

A

alveoli and airways in the entral acinus, destroying alveoli in the walls of respiratory bronchioles and alveolar ducts

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5
Q

panacinar

A

affects whole acinus

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6
Q

paraseptal

A

basic lesion of pulmonary bullous

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7
Q

acinus

A

whole funcitonal unit of alveoli and alveolar ducts

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8
Q

alveoli

A

air pockets lining respiratory airways

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9
Q

what happens in emphysema

A

Primarilu alveoli and small distal airways are affected by the disease and followed by effects in larger airways​

Elastic recoil usually responsible for splinting bronchioles open but bronchioles lose their stabilising functioon and cause collapse in airways, results in gas trapping distally ​

Erosion in lveolar septa​

Enlargement of available air space ​

Sometimes formation of bullae with their thin walls ​

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10
Q

how does smoking affect emphysema

A

Smoking?​

Initally activates inflammatory response ​

Causes inflammatory cells to be released from polymorphonuclear leukocytes and alveolar macrophages to move into the lungs​

Lungs are usually protected against proteolytic enzymes ​

Anti proteases such as alpha1-antitrypsin reduces its activity ​

Develops in this situation when production and activity of antiprotease arent sufficient to counter harmful effects of excess protease production ​

Destruction of alveolar walls and breakdown of elastic tissue and collagen ​

Loss of this tissue leads to reduction of surface area for gas exchange ​

Increases rate of blood flow through the pulmonary capillary system ​

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11
Q

definition of chronic bronchitis

A

chronic cough and sputum production for at least 3 months a year for 2 consecutive years

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12
Q

chronic bronchitis pathophysiology

A

Caused by overporduction and hypersecretion of mucus by goblet cells ​

Epithelial cells lining the airway respond to toxic, nfectious stimuli by releasing inflamamtory mediators and pro-inflammatory cytokines ​

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13
Q

acute exacerbation of chronic bronchitis

A

Bronchial mucours membrane becomes hyperemic and edematous with diminished bronchomucociliary function ​

Impediment because of luminal obstruction to small airways​

Airways clogged by debris causing further irritation ​

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14
Q

characteristic cough of chronic bronchitis

A

opious secretion of mucus

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15
Q

common COPD symptoms

A

Shortness of breath – may only happen when exercising at first​

A persistent chesty cough with phlegm that does not go away​

Frequent chest infections​

Persistent wheezing​

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16
Q

what may a GP do to diagnose COPD

A

Ask you about your symptoms​

Examine your chest and listen to your breathing using a stethoscope​

Ask whether you smoke or used to smoke​

Calculate your body mass index (BMI) using your weight and height​

Ask if you have a family history of lung problems

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17
Q

diagnosing COPD

A

GP
spirometry
chest x ray
blood tests
potential other tests

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18
Q

spirometry

A

A spirometry test can help show how well your lungs are working.​

You’ll be asked to breathe into a machine called a spirometer after inhaling a bronchodilator.​

The spirometer takes two measurements: the volume of air you can breathe out in a second, and the total amount of air you breathe out. You may be asked to breathe out a few times to get a consistent reading.​

The readings are compared with normal results for your age.

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19
Q

chest x ray

A

Can be used to look for problems in the lungs that can cause similar symptoms to COPD.​

Problems that can be shown by an X-ray include chest infections and lung cancer, although these do not always show.

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20
Q

blood test

A

A blood test can show other conditions that cause similar symptoms to COPD such as anaemia and erythrocytosis.​

Sometimes a blood test may be don’t to see if you have alpha-1-antitrypsin deficiency, a rare test that increases your risk of COPD.

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21
Q

further tests in diagnosis

A

electrocardiogram
echocardiogram
peak flow test
blood oxygen test
ct
phlegm sample

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22
Q

MDT involved in COPD

A

Pulmonologist​

Pulmonary rehabilitation therapist​

Pharmacist​

Mental health therapis​

Nutritionist or Dietician​

Thoracic surgeon​

Palliative care team

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23
Q

effect of smoking on respiratory system, histologically

A

bronchial epithelium
goblet cells
cilia
inflammation
lung parenchyma

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24
Q

bronchial epithelium

A

metaplasic
transformaton of normal cilitated pseudostratfied columnar
to squamous metaplasic

reduced effectiveness of mucociliary clearance

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25
goblet cells
smoking increases number and activity of goblet cells goblet cells produce excess mucus which produces thick, sticky layer of mucus can accumulate in airways and contribute to chronic bronchitis and higher risk of respiratory infections
26
cilia
damaged impair ciliary function by toxins in smoke reduce efficacy to clear mucus and particles in lungs increased risk of resp infections
27
inflammation
induces chronic inflammation in resp tract inhaled toxins in cigarette smoke triggers an immune response of neutrophils and macrophages damages resp tissue
28
lung parenchyma
destruction of alveolar walls enlarged air spaces loss of elasticity reduces surface area for gas exchange
29
effect of smoking on caridovascular system
coronary heart disease stroke heart attack/myocardial infarction peripheral vascular disease
30
nicotine and free radicals in smoe
alter expression and activity of NO synthase react with NO decrease NO availability normally NO is involved in vasodilation so blood vessels remain contracted increases blood pressure
31
nicotine
sympathetic stimulaiton increase in heart rate and blood pressure
32
carbon monoxide
irreversibly binds to haemoglobin prevents oxygen transport decreased perfusio of tissues with oxygen
33
oxidant gases and free radicals
in cigarettes and secreted by immune cells in response to non-self molecules cause oxidative stress as their unpaired electrons make them hghly reactive damage molecules and cells changing their structure and function damages endothelial cells of blood vessels inflammation
34
NO what does it do
inhibit platelet secretion reducing NO increases platelet secretion possible thrombus formation
35
increasing LDL and HDL
increased levels of free cholesterol in blood build up under endothelial lining causing atherosclerosis
36
damage to endothelum
promotes thrombosis activation and aggregation on platelets activation of coagulaiton factors (thrombin and fibrinogen) decreased fbrinolysis
37
common cancers that smoking increases the risk of
mouth throat laryngeal oesophageal bladder bowel cervical kindey liver stomach pancreas
38
carcinogens cigarette smoe
over 60 known pro-carcinogens metabolised in the body to become carcinogenic catalysed by cytochrome P450
39
DNA adducts, carcinogens
adducts covalently bind to the DNA causing change in structure if DNA isnt repaired before synthesis then mutations ocur DNA polymerase wll insert the wrong base transition mutation occurs (pyrimidine for purine) or transversion (purine for pyrimidine) covalent binding of DNA adducts can result in strand breaks can lead to deletion mutation causing frame shifts non-functional protein formation
40
what may DNA mutations also do
activate proto-oncogenes or inactivate tumour suppressor genes uncontrolled replication and possible cancer
41
NICE diagnossi
symptoms MCR dysnopea scale spirometry x ray ct
42
treatment 1st line NICE
smoking cessation information about the disease pneumococcal and influenxa vaccine pulmonary rehabilitation if needed treatment for associated comorbitidies self management plan
43
when would someone be referred to respiratory specialist
lung cancer or bronchiectasis suspected under 40 family history of alpha-1-antitrypsin deficiency oxygen therapy, long term non invasive ventilation therapy, long term oral corticosteroids or lung surgery
44
what is offered in treatment if needed
SABA SAMA
45
if person has asthma symptoms
consider LABA and ICS if not wroking then LABA LAMA and ICS
46
non asthmatic features
LABA and LAMA if they have 1/2 exacerbations or day to day symptoms impacting quality of life offer LABA, LAMA and ICS
47
SABA
salbutamol
48
SAMA
ipratroprium
49
asthmatic features classification
patients FEV is less than 50
50
LABA
salmetarol
51
ICS
inhaled corticosteroid budesonude
52
B2 receptors
n lungs respond to adrenaline allow dilation of bronchiolar smooth muscle
53
muscarinic antagonists
increase airflow blocking cholinergic tone at airway smooth muscle
54
pulmonary rehabilitation
frst part of session is exercise second is information guidance Exercise and education programme designed for people with lung disease who experience symptoms of breathlessness.​ ​ improve your muscle strength so you can use the oxygen you breathe more efficiently​ cope better with feeling out of breath​ improve your fitness​ improve your mental wellbeing ​ help you feel less tired ​ reduce your risk of being admitted to hospital with a chest infection or flare-up​ help you understand and manage your condition better.
55
methods of smoking cessation
prescription medication: bupropion, varenicline nicotine replacemetn therapy e cigarettes/ vaping
56
bupropion
MOA: Inhibits the reuptake of dopamine, noradrenaline, and serotonin in the CNS, reducing the nicotine withdrawal symptoms.​ Originally used to treat depression.​ Only available on prescription.​ 1 to 2 tablets are taken a day for the course of 7 to 9 weeks.
57
who cant use brupropion
Children under the age of 18​ -women who are pregnant or breastfeeding ​ -People with epilepsy, bipolar disorder or eating disorders​ ​ ​
58
varenicline
-reduces the cravings for nicotine ​ -Blocks the rewarding and reinforcing effect of smoking​ ​ MOA: partial agonist of the nicotine receptors in the brain. It binds to these receptors, stimulating them partially and also blocking the effects of nicotine if a person smokes while taking the medication. ​ Dual effect: helps to reduce cravings and withdrawal symptoms.
59
varenicline extra info
currently not used in UK
60
aim of NRT
Aim: reduce withdrawal symptoms and cravings associated with smoking, making it easier for the individuals to quit smoking. ​ It is a medicine which provides you with a low level of nicotine, without the harmful toxins present in tobacco smoke (tar, carbon monoxide)
61
what is NRT available as
-skin patches​ -chewing gum ​ -inhalators ​ -tablets ​ -nasal and mouth spray
62
e cigarettes and vaping
It is a device that allows you to inhale nicotine in a vapour rather than smoke.​ They work by heating a liquid (containing nicotine).
63
how are e cigarettes better than smoking
-They do not burn tobacco, therefore do not produce tar or carbon monoxide.​ -The liquid and vapour contains some potentially harmful chemicals found in cigarette smoke, but at a much lower level.
64
social factors initiating smoking
peer pressure social acceptance nfluence exposure through media or advertising
65
psychological factors for intiating smoking
curiosity rebellion desire for risk taking and self expression way to cope
66
social factor maintaining smoking
social environment being around people who smoke
67
psychological factors for maintaining smokng
nicotine addiciton dependence on smoking habit formation perception of smoking as a coping mechanism
68
social factors stopping smoking
social support encouragement positive role models positive social pressure
69
psychological factors for stopping smoking
personal motivation and readiness save money improving health regain control on life
70
why should you seek help with smoking
increased success in quitting support and guidance healt hbenefits addressing nicotine addiction emotional support
71
what is second hand smoke
tobacco smoke that affects non smoker from cigarette end as sidestream smoke or exhaled by the person smoking
72
pregnancy and passive smokng
baby more at risk of low birthweight and sudden infant death syndrome
73
new law with smoking
illegal to smoke in private vehicle if person under 18 present
74
children who live in household where 1 person smokes are more likely to develop what
asthma chest infections meningitis ear infections coughs and colds
75
depression and smoking
nicotine stimulates release of dopamne involved in triggering positive feelings found to be low in people with depression may then use cigarettes to temporarily increase dopamine supply
76
strategies to smoking cessation
3 week cough campagin NRT behavoural support social support smoke free envronments SMART goals offer incentives ongoing suppor.t smoking cessation clinics
77
smoking cessation clinics
free service 12 weeks motivational interviewing give accurate infromation and support breath test
78
be clear on cancer 3 week cough campaign
encourages people to go to the GP if you have had a cough for longer than 3 weeks make lung cancer symptoms aware 70% lung cancers diagnosed at late stage higher rate of survival if diagnosed earlier
79
barriers to smoking cessation
nicotine addiction lack of motivation or readiness fear of withdrawl symtposm social influences stress and copinig mechanism lack of support or encouragement from family previously uncuccessful advertising and marketing of smoking campaign accessbility of tobacco products co-existing mental conditions
80
smoking trends
men more likely higest in age 25-34 no qualifications are more likely to be current smokers than those with higher levels of education unemployed higher rates than employed