Unit 8 Case 3: COPD Flashcards
what is COPD
Chronic obstructive pulmonary disease
Umbrella term for a group of lung conditions that cause breathing difficulties
2 main conditions involved in COPD
emphysema
chronic bronchitis
3 different types of emphysema
centriacinar
panacinar
paraseptal
centriacinar
alveoli and airways in the entral acinus, destroying alveoli in the walls of respiratory bronchioles and alveolar ducts
panacinar
affects whole acinus
paraseptal
basic lesion of pulmonary bullous
acinus
whole funcitonal unit of alveoli and alveolar ducts
alveoli
air pockets lining respiratory airways
what happens in emphysema
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
how does smoking affect emphysema
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
definition of chronic bronchitis
chronic cough and sputum production for at least 3 months a year for 2 consecutive years
chronic bronchitis pathophysiology
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
acute exacerbation of chronic bronchitis
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
characteristic cough of chronic bronchitis
opious secretion of mucus
common COPD symptoms
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
what may a GP do to diagnose COPD
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
diagnosing COPD
GP
spirometry
chest x ray
blood tests
potential other tests
spirometry
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.
chest x ray
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.
blood test
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.
further tests in diagnosis
electrocardiogram
echocardiogram
peak flow test
blood oxygen test
ct
phlegm sample
MDT involved in COPD
Pulmonologist
Pulmonary rehabilitation therapist
Pharmacist
Mental health therapis
Nutritionist or Dietician
Thoracic surgeon
Palliative care team
effect of smoking on respiratory system, histologically
bronchial epithelium
goblet cells
cilia
inflammation
lung parenchyma
bronchial epithelium
metaplasic
transformaton of normal cilitated pseudostratfied columnar
to squamous metaplasic
reduced effectiveness of mucociliary clearance
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
cilia
damaged
impair ciliary function by toxins in smoke
reduce efficacy to clear mucus and particles in lungs
increased risk of resp infections
inflammation
induces chronic inflammation in resp tract
inhaled toxins in cigarette smoke triggers an immune response of neutrophils and macrophages
damages resp tissue
lung parenchyma
destruction of alveolar walls
enlarged air spaces
loss of elasticity
reduces surface area for gas exchange
effect of smoking on caridovascular system
coronary heart disease
stroke
heart attack/myocardial infarction
peripheral vascular disease
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
nicotine
sympathetic stimulaiton
increase in heart rate and blood pressure
carbon monoxide
irreversibly binds to haemoglobin
prevents oxygen transport
decreased perfusio of tissues with oxygen
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
NO what does it do
inhibit platelet secretion
reducing NO increases platelet secretion
possible thrombus formation
increasing LDL and HDL
increased levels of free cholesterol in blood
build up under endothelial lining
causing atherosclerosis
damage to endothelum
promotes thrombosis
activation and aggregation on platelets
activation of coagulaiton factors (thrombin and fibrinogen)
decreased fbrinolysis
common cancers that smoking increases the risk of
mouth
throat
laryngeal
oesophageal
bladder
bowel
cervical
kindey
liver
stomach
pancreas
carcinogens cigarette smoe
over 60 known
pro-carcinogens
metabolised in the body to become carcinogenic
catalysed by cytochrome P450
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
what may DNA mutations also do
activate proto-oncogenes
or inactivate tumour suppressor genes
uncontrolled replication and possible cancer
NICE diagnossi
symptoms
MCR dysnopea scale
spirometry
x ray
ct
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
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
what is offered in treatment if needed
SABA
SAMA
if person has asthma symptoms
consider LABA and ICS
if not wroking then LABA LAMA and ICS
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
SABA
salbutamol
SAMA
ipratroprium
asthmatic features classification
patients FEV is less than 50
LABA
salmetarol
ICS
inhaled corticosteroid
budesonude
B2 receptors
n lungs
respond to adrenaline
allow dilation of bronchiolar smooth muscle
muscarinic antagonists
increase airflow
blocking cholinergic tone at airway smooth muscle
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.
methods of smoking cessation
prescription medication: bupropion, varenicline
nicotine replacemetn therapy
e cigarettes/ vaping
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.
who cant use brupropion
Children under the age of 18
-women who are pregnant or breastfeeding
-People with epilepsy, bipolar disorder or eating disorders
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.
varenicline extra info
currently not used in UK
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)
what is NRT available as
-skin patches
-chewing gum
-inhalators
-tablets
-nasal and mouth spray
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).
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.
social factors initiating smoking
peer pressure
social acceptance
nfluence
exposure through media or advertising
psychological factors for intiating smoking
curiosity
rebellion
desire for risk taking and self expression
way to cope
social factor maintaining smoking
social environment
being around people who smoke
psychological factors for maintaining smokng
nicotine addiciton
dependence on smoking
habit formation
perception of smoking as a coping mechanism
social factors stopping smoking
social support
encouragement
positive role models
positive social pressure
psychological factors for stopping smoking
personal motivation and readiness
save money
improving health
regain control on life
why should you seek help with smoking
increased success in quitting
support and guidance
healt hbenefits
addressing nicotine addiction
emotional support
what is second hand smoke
tobacco smoke that affects non smoker
from cigarette end as sidestream smoke
or exhaled by the person smoking
pregnancy and passive smokng
baby more at risk of low birthweight and sudden infant death syndrome
new law with smoking
illegal to smoke in private vehicle if person under 18 present
children who live in household where 1 person smokes are more likely to develop what
asthma
chest infections
meningitis
ear infections
coughs and colds
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
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
smoking cessation clinics
free service
12 weeks
motivational interviewing
give accurate infromation and support
breath test
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
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
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
