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
Q

goblet cells

A

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

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26
Q

cilia

A

damaged
impair ciliary function by toxins in smoke
reduce efficacy to clear mucus and particles in lungs
increased risk of resp infections

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27
Q

inflammation

A

induces chronic inflammation in resp tract
inhaled toxins in cigarette smoke triggers an immune response of neutrophils and macrophages
damages resp tissue

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28
Q

lung parenchyma

A

destruction of alveolar walls
enlarged air spaces
loss of elasticity
reduces surface area for gas exchange

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29
Q

effect of smoking on caridovascular system

A

coronary heart disease
stroke
heart attack/myocardial infarction
peripheral vascular disease

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30
Q

nicotine and free radicals in smoe

A

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

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31
Q

nicotine

A

sympathetic stimulaiton
increase in heart rate and blood pressure

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32
Q

carbon monoxide

A

irreversibly binds to haemoglobin
prevents oxygen transport
decreased perfusio of tissues with oxygen

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33
Q

oxidant gases and free radicals

A

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
Q

NO what does it do

A

inhibit platelet secretion
reducing NO increases platelet secretion
possible thrombus formation

35
Q

increasing LDL and HDL

A

increased levels of free cholesterol in blood
build up under endothelial lining
causing atherosclerosis

36
Q

damage to endothelum

A

promotes thrombosis
activation and aggregation on platelets
activation of coagulaiton factors (thrombin and fibrinogen)
decreased fbrinolysis

37
Q

common cancers that smoking increases the risk of

A

mouth
throat
laryngeal
oesophageal
bladder
bowel
cervical
kindey
liver
stomach
pancreas

38
Q

carcinogens cigarette smoe

A

over 60 known
pro-carcinogens
metabolised in the body to become carcinogenic
catalysed by cytochrome P450

39
Q

DNA adducts, carcinogens

A

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
Q

what may DNA mutations also do

A

activate proto-oncogenes
or inactivate tumour suppressor genes
uncontrolled replication and possible cancer

41
Q

NICE diagnossi

A

symptoms
MCR dysnopea scale
spirometry
x ray
ct

42
Q

treatment 1st line NICE

A

smoking cessation
information about the disease
pneumococcal and influenxa vaccine
pulmonary rehabilitation if needed
treatment for associated comorbitidies
self management plan

43
Q

when would someone be referred to respiratory specialist

A

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
Q

what is offered in treatment if needed

A

SABA
SAMA

45
Q

if person has asthma symptoms

A

consider LABA and ICS
if not wroking then LABA LAMA and ICS

46
Q

non asthmatic features

A

LABA and LAMA
if they have 1/2 exacerbations or day to day symptoms impacting quality of life offer LABA, LAMA and ICS

47
Q

SABA

A

salbutamol

48
Q

SAMA

A

ipratroprium

49
Q

asthmatic features classification

A

patients FEV is less than 50

50
Q

LABA

A

salmetarol

51
Q

ICS

A

inhaled corticosteroid
budesonude

52
Q

B2 receptors

A

n lungs
respond to adrenaline
allow dilation of bronchiolar smooth muscle

53
Q

muscarinic antagonists

A

increase airflow
blocking cholinergic tone at airway smooth muscle

54
Q

pulmonary rehabilitation

A

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
Q

methods of smoking cessation

A

prescription medication: bupropion, varenicline
nicotine replacemetn therapy
e cigarettes/ vaping

56
Q

bupropion

A

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
Q

who cant use brupropion

A

Children under the age of 18​

-women who are pregnant or breastfeeding ​

-People with epilepsy, bipolar disorder or eating disorders​

58
Q

varenicline

A

-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
Q

varenicline extra info

A

currently not used in UK

60
Q

aim of NRT

A

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
Q

what is NRT available as

A

-skin patches​

-chewing gum ​

-inhalators ​

-tablets ​

-nasal and mouth spray

62
Q

e cigarettes and vaping

A

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
Q

how are e cigarettes better than smoking

A

-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
Q

social factors initiating smoking

A

peer pressure
social acceptance
nfluence
exposure through media or advertising

65
Q

psychological factors for intiating smoking

A

curiosity
rebellion
desire for risk taking and self expression
way to cope

66
Q

social factor maintaining smoking

A

social environment
being around people who smoke

67
Q

psychological factors for maintaining smokng

A

nicotine addiciton
dependence on smoking
habit formation
perception of smoking as a coping mechanism

68
Q

social factors stopping smoking

A

social support
encouragement
positive role models
positive social pressure

69
Q

psychological factors for stopping smoking

A

personal motivation and readiness
save money
improving health
regain control on life

70
Q

why should you seek help with smoking

A

increased success in quitting
support and guidance
healt hbenefits
addressing nicotine addiction
emotional support

71
Q

what is second hand smoke

A

tobacco smoke that affects non smoker
from cigarette end as sidestream smoke
or exhaled by the person smoking

72
Q

pregnancy and passive smokng

A

baby more at risk of low birthweight and sudden infant death syndrome

73
Q

new law with smoking

A

illegal to smoke in private vehicle if person under 18 present

74
Q

children who live in household where 1 person smokes are more likely to develop what

A

asthma
chest infections
meningitis
ear infections
coughs and colds

75
Q

depression and smoking

A

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
Q

strategies to smoking cessation

A

3 week cough campagin
NRT
behavoural support
social support
smoke free envronments
SMART goals
offer incentives
ongoing suppor.t
smoking cessation clinics

77
Q

smoking cessation clinics

A

free service
12 weeks
motivational interviewing
give accurate infromation and support
breath test

78
Q

be clear on cancer 3 week cough campaign

A

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
Q

barriers to smoking cessation

A

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
Q

smoking trends

A

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