Lecture 8: Obstructive Lung Disease Flashcards
What is obstructive lung disease
Can’t get air out
What is restrictive lung disease?
Can’t get air in
Most common obstructive lung disease
COPD (often used as an umbrella term)
KNOW: For asthma you have increased mucus where the broncioles are
* mostly classified as obstructuive
In emphysema its hard to get their air out because the alveoli are going to collapse and trap gas inside
Chronic bronchititis is hypesecrtion of mucus in the bronchus
What are the different obstructive pulmonary diseases
A - Asthma
B - Bronchiectasis
C - Cystic Fibrosis/Chronic Bronchitis
D - Decreased FEV1/FVC ratio
E - Emphysema
What 3 things does Spirometry consist of (3)
1) Forced vital capcity
2) Forced expiratory volume exhaled in the first second (FEV1)
3) FEV1/FEV ratio = this is typically what we use to tell if its restrictive or obstructive
What is a normal FEV1/FVC ratio?
* also FEV1 and FVC have to be above __ of perdicted value
FEV1/FVC ratio > 0.70
* because we expell most of what we breath in in the first second
FEV1 AND FVC above 80% of the perdicted value
What are the 4 clinical manifestations of chronic obstructive pulmonary disease (COPD)
Risk factors (2)
GOLD Guidelines
1) Increased resistance to airflow
2) Abnormal breathing sounds
3) Use of accessory muscle (because they are hyperinflated they are going to need more effort to expire are - so you need more accessory muscles)
4) Dry or productive cough
* Productive = white, clear, yellow
Risk factors
* Smoke
* 40+
GOLD standards are what
what to do for COPD
These are pulmonary function tests
Blue = normal
Red = Obstructive pattern
Notice you’re not expelling as much of it out
* decreased expiration
You also can’t get as much air in because you didnt get it all out
With obstruction
* we see that ratio is less than 0.7
You can see the amount that is expelled in that first second is very minimal compared to a normal lung
* you’re getting a lot out very slowly
How to classify COPD
* guides management / regulations for PT / medicine
* You can see its dervivied from those spirometry #’s
Memorize these classifications
Note #1 is over 80% of perdicted which is normal, however they’re still having symptoms so we classify as mild
* they are expected to progress - theres something else indicating they have COPD
Dyspnea scale
COPD can be stable and it can have flare ups
the below is what to do for stable COPD
NOTE: now they’re at high risk for infection / mortality
* common colds will be more aggressive because of comprimsied lung system
How to help a patient quit smoking
Pulmonary rehab typically ran by nurses and EX phsyiologist
Detailed program for programs w/ certain qualifying diagnosis
Goal is to basically do what we do except w/ the lungs
help them avoid COPD exacerbtions
KNOW: The underlying cause of COPD is not treated
* However, the medications are aimed at treating the symptoms - which is airway obstruction
Why do we use beta adergenic drugs for COPD?
* What kind of beta blockers
* What 4 drugs are this?
Beta-Adergenic
* stimulates beta 2 receptors in relaxation of bronchile smooth muscle (has opposite affect in lungs I think)
Increases the activity of the adenyl cyclase enzyme
* The increase protein kinase activity ultimately inhibits smooth-muscle contraction
* cAMP is the second messenger that brings about respiratory smooth-muscle relaxation and subsequent bronchodilation
Administered orally, subcutaneously, or inhalation (preferred) - Nebulizer or metered-dose inhalers
Meter dose: a quick puff
nebulizer: like a mask that goes over
Drugs:
* Albuterol
* Arformoterol
* Epinephrine
* Formoterol
Using it a lot = does the opposite of what we want it to do
Adverse effects of Beta-Adergenic drugs for COPD (3)
1) w/ prolonged or excessive use, inhaled adrenergic agonists may actaully increase bronchial responses to allergens and other irritants
2) Adrenergic agonists that also stimualte beta 1 recptors may cause cardiac irregularitites if they reach the myocardium through the systemic circulation
3) Stimulation of CNS adrenergic receptors may produce symptoms of nervousness, restlessness, and tremor
For COPD we try to increase the vasodilation within the bronchile
We also use the anti inflammatory steriod because theres mucus in this response
I think its a combo of the two
Symbicort very common
Inflammatory compounds that are especially important in mediating the airway inflammation that underlies bronchoconstrictive disease
Why are the perfurfed
MOA
Leukotrienes
Low adverse effects
Luelotrine inhibitors Inhibit the lipoxygenase enzyme, thereby reducing the production of leukotrines
Luekitriene inhibitors are used to reduce the produion of leukotrines, which are inflammatory compounds that contribue to airway inflammation and bronchoconstirciton in conditions like asthma.
What drugs block muscarinic cholinergic receptors and prevent acetylcholine induced bronchoconstriction, thus improing airflow in certain types of bronchospastic disease
Anticholinergics
so the decrease those bronchospasms
Most common anticholinergics
Spiriva
KNOW: any drug thats inhaled, the adverse effect is dry mouth
* you’re inhaling something that does vaso constriction
* And the salvairy glands vasoconstrict = decrease salvia = give them water
Side effects w/ anticholinergics (6)
Due to CNS activation
1) dry mouth
2) Constipation
3) Urinary retention
4) Tachycardia
5) Blurred vision
6) Confusion
What do Xanthine Derivatives do?
* MOA
* Why cant you take these for long
Produce bronchodilation in asthma and other forms of airway obstruction
THEY ARE BRONCHODILATORS
Inhibit the phosphodieterase enzyme located in bronchial smooth muscle cells
* PDE break down CAMP; inhibiting this enzyme results in higher intracellular cAMP concentration
cAMP is the second messenger that brings about respiratory smooth-muscle relaxation and subsequent bronchodilation
You cant use these that much because they have a high toxivity
* recommended theraputic lvls = 10-20 micograms
* toxiicity = 15
* Therpautic range is in the toxic range = bad
* dont take long term because they can build up in system
Recommended levels for xanthine derivatives
* what is the most serious limitation in the use of these
10-20 ug/mL
most serious = toxicity
NOTE: over 15 - toxicity may appear
when blood levels exceed 20 ug/mL serious side effects such as cardiac arrhythmias and seziures may occur
Theophylline-induced seizures are a life threatning phenomenon
Utilize lowest possible dose
Xanthine Derivative Bronchodilators
What do zanthine derivatives end in?
lline
z
These are steriods
* mostly one
have to be careful using these because they are glucosteriods which increase glucose - bad w/ diabetes
COPD has mucus + bronchosmpasms
* we need to preven these
GOAL for treating: Maintaining airway patency and preventing airflow restriction
KNOW theophylline is used for COPD but is a xanthine deriviative (so have to be careful)
Long acting beta adergenc (LABA)
LAMA
in combination
mild
* LABA+LAMA
* or just bronchodilator
gold classification
First thing to look at with inhalers is to look at how theyre administering it
* ejucate there
Be able to dilinate long acting and short acting inhaled bronchodilators
Inhaled corticosteriods is list from earlier
Which of the following drugs is used to prevent or reverse bronchial constriction and subsequent obstruction of the airway in the lungs
1) Beta-adergenics
2) Antitussives
3) Antihistamines
4) Mucolytics
Beta-adergenics is the answer
* Increases bronchodilation
Antitussives: used to reduce cough
Antihistamines: For inflammation / immune response / allergies
Mucolytics: break up mucus
Increased reactivity of the trachea and bronchi to various stimuli causing widespread narrowing of the airway due to inflammation, smooth muscle constriction, and increased secretions
* what kind of muscle contracts
risk factors
Asthma
KNOW: Response can be immediate or delayed
Bronchial smooth muscle constriction
Mucus production (without infection) resulting from the increased presence of leukocytes, such as eosinophils
Bronchial mucosa inflammation and thickening resulting from cellular and fluid infiltration
Risk factors:
* age
* heredity
* smoking
* maternal use of antibiotics in third trimester
* low birth weight
* viral infections before 3
* Low socical economic status (somewhere w/ fumes)
* cockroach/rodent infestation
Clinical manifestation of asthma (4)
1) Wheezing cough
2) Dry or productive sputum with plugs (mucus getting stuck –> leads to infection)
3) Anxiety
4) Decreased chest wall symmetry
asthma
In the past, treatment consisted primarily of bronchodilators such as the beta-adrenergic agonist and the xanthine derivities
* glucocorticoids were added only in more advanced and severe cases
* Glucocorticoids, however, are now used as first-line agents in most patients, included cases of newly detected, mild asthma
Glucocorticoids are used to control inflammation mediated bronchospasm
* most effective agents for controlling asthma
* Directly affects the genes and transcription factors that produce inflammatory components
Adverse effects of glucocorticoids
because of the general catabolic effect of these drgs on supporting tissues, problems with osteoporisis, skin breakdown, and muscle wasting can occur during prolonged systemic administration
Retardation of growth in children, cataracts, glaucoma, hyperglycemia, aggravation of diabetes mellitus, and hypertension
Long term management of asthma
Glucocorticoids directly affect the underlying disease process by decreasing the inflammation causing airway hyperresponsiveness
Glucocorticoids can also be combined with a long acting beta 2 agonist to provide optimal results (LABA)
* Glucocorticoids can help decrease the inflammatory response that causes airway hyperresponsiveness, while the beta 2 drug maintains brochodilation in people with asthma
Short acting beta 2 agonist act as “rescue” therapy at the onset of a bronchospastic attack (SABA)
* typically for EX induced astham
anti inflamatory steriod combination in combination with long acting beta 2 bronchodilator (management of asthma)
* Advair
* Symbicort
* dulera
* all very common
LABA = ol
When do you use cromones for asthma?
* what do they do
* What do they do to mast cells?
Use prior to an attack
Cromolyn sodium and other cromones are believed to prevent bronchoconstriction by inhibiting the release of inflammatory mediators
Mast cells stabilizers
* like little bombs that have hisatmines etcs
* They have receptors for your allergines on there
* when they come into contact w/ that allergine they release all their contents
* They’re everywhere, on skin, inside body etc.
* When one is activated they activate all over your body
* So cromones keep these from opening
Cromones side effects
really not many
some irrtation of the nasal and upper respiratory passaes may occur follow inhalation
* because its inhaled
Cromolyn sodium is often used to treat seasonal allergies
* treating mild persistent asthma in children
* People who are unable to tolerate the side effects of those antiasthma drugs
Which of the following is an adverse effect of glucocorticoids
1) they are relatively free of adverse effects
2) Seizures
3) Accelerated growth
4) Increased blood glucose
4
this is why you have to be careful if they have diabetes
Obstructive, restrictive disorder; permanent dilation of airways that have a normal diameter of greter than 2 mm
* etilogy
* pathogensis
Bronchiectasis
* Both obstructive and restrictive
* can cause airway to collapse on itself, which is why its obstrutive
Previous bacterial respiratory infection, CF, tuberculosis (TB), chronic aspiration, and immobile cilia syndromes
Pthogensis
* Destruction of the elastic and mscular bronchiole walls
* Destruction of the muccociliary escalator (in which normal epithelium is replaced by nonciliated mucus-prpducing cells) - mucus not being able to move out
* Bronchial dilation
* Bronchial artery enlargement
Chronic inflammation and scarring of the bronchial lining with cough and sputum production lasting at least 3 months for 2 consecutive years
Risk factor:
clinical manifestations
treatment
Chronic Bronchitits
* Key is that it lasts at least 3 months for 2 years
* takes a while
Risk factor: Smoking
Clinical manigestations:
* Wheezing or rhonchi breath sounds
* Productive mucoid or purulent sputum with infection
* May have fever - because you have an infection
* Abnormal V/Q matching and decreased PaO2 (ventilation perfusion ratio) - mismatch of the amount of air in and gas exchange
Treatment:
* Pulmonary hygiene - think chest massage
* Paced breathing
* Endurance - endurance that increases function
* Patient education (maybe stop smoking)
chronic bronchitits is often termed blue bloater
* Stock build and depdent edema
* Tachypnea with prolonged expiratory phase (matched fev1 ratio –> much longer and prolonged because they arent getting out all the air they should in that first 1 seconds)
* accessory muscle use w/ fixed UE
* Elevated shoulders
* Barrel chet
* fatigue
* anxiety (because you cant get enough air out)
Enlargement of the air spaces beyond the terminal bronchiole (so i guess enlargement of alveoli), loss of elasticity in distal airways, airway collapse,and gas trapping
* 2 causes
Emphysema
Causes:
* Genetic - lack of proteolytic inhibitors allows the alveolar interstitium to be destroyed
* It may be caused by cigarrete smoking, air pollutatnts, or infection
black spots shouldnt be there
Three types of emphysema
* most common
Centrilobular - most common - affects the upper growths
Panlobular
Pariseptal
What happens to the alveoli walls w/ emphasima
progressive destruction
* decreased elasticity
* Premature airway collapse
* Bullae formation (a bulla is a pocket of air surrounded by walls of compressed lung parenchyma) - think the air bubbles on the pizza - trapped air surrounded by compressed lung tissue
Clinical manifestation w/ emphysema (5)
Treatment (5)
Manifestation:
1) Barreled chest - pink puffer
2) Use of accessory muscles of ventilation
3) Diminished breath sounds
4) Dyspnea
5) Chronic cough
Treatment
1) Pursed lip breathing
2) Patient education
3) Endurance exercises
4) Lung transplant
5) Lung volume reception surgery (cut parts of the lung that are damaged)
Smoking is a major compoenent of both
This is the barrel chest look w/ emphysema
notice the white cloudy look
What is the leading risk factor for emphysema
1) Prolonged steriod use
2) Smoking
3) Respiratory failure
4) Genetic Origin
D
Smoking is one, but genetic is leading cause
Exercise-Induced bronchospasm or bronchoconstriction
Acute, reversible airway obstruction that occurs 5-15 minutes after vigorous exercise
* risk factors
* etiology
* Symptoms
* treatment
Risk factors:
* asthma
* female
* winter sports
* exercise in dry air
* chloramines in wter
* emission from ice cleaning equipment
* pollution
* endurance sports
Etiology: increased RR decreased humidification - that increased RR is going to lead to decreased humidification (nasal cavity)
* Mast cells degranulate and release leukotrines, hisatmine, tryptase, prostaglandins, and eosinophils (all those things are in that little massed cell bomb)
Symptoms:
* Wheezing, dyspnea, cough, chest tightness, and mucus production during or after EX
Treatment: SABA prior to EX < 4x/week; warm-up
* if using inhaler more than 4x per week thats a problem
Sleep disordered breathing (think sleep apnea)
Collection of syndromes characterized by breathing abnormalitties during sleep (3)
These sleep disorders occur in how much of the population?
* which sex has it more
* neck circumference > what for women and men
risk factors
clinical manigestations (5)
1) Cheyne-Stokes respiration
2) Hypoventilation syndrome
3) Obstructive sleep apnea
2-4% of pop
men have it more
neck 16in for women
neck 17in for men
Risk factors: obesiy, cardiac conditions, older age, male, AA or Asian decent, alcohol use may make it worse
clinincal manifestations:
* HR and BP elevation
* Elevated inflammatory markers
* Elevated glucose levels (due to fight or flight which mobilizes blood glucose)
* HTN, low CO
Rehab for COPD
Breathing EX
Airway clearance
Physical training
* Upper extremities
* Aerobic and strengthening
* Activities they enjoy
Posture
Conditioning of respiratory musculature
Inspiratory muscle training, spirometry
Pacing and energy conservation
Functional walk testsL 6 MWT, 2MWT, 2MST
60%-80% Hrmax
BP and pulse observed at rest, and in response to therEx
O2 state > 90%
Inherited disorder of ion transportation (sodium and calcium) in exocrine glands
* what systems involved
Do they develop obstructive or restrictive lung disease?
pathogensis?
Cystic fibrosis
Liver, GI, respiratory, and reproductive involvement
Chronic bacterial airway infections is typically how they get diagnosed
* now they have genetic testing to tell this
Develop obstructive lung disease due to that increased mucus production
Pathogensis:
* Epithelial cells are impermeable to chloride
* Leads to dehydrated gland cells, increased mucus production (dehydration leads to increased mucus production, body trying to compensate)
* Elevation of sweat electrolytes - because you’re not using these electrolytes they go to sweat
* Pancreatic enzyme insufficiency (because thats an exocrine gland)
Where does cystic fibrosis primarily affect the lungs?
Bronchioles
KNOW: w/ cycstic fibrosis both parents must be carries of the defective gene
Early stages of cystic fibrosis
* how does cough start?
Persistent cough, sputum production, presistent wheezing, recurrent pulmonary infections
Salty skin and sweat (becuase those ions are in the sweat now), excessive appetite but inability to gain wt (because of the pancreatic enzyme insufficency - you are not absorbing all the nutrients from food, so your body thinks your malnurished but you cant gain wt), bulk, foul smelling stools (makes sense, everything isnt being absorbed)
Initially, dry, non productive cough
Advanced stage cystic fibrosis
Barrel chest
kyphosis
clubbing
bronchitits
pneumothorax (one of your lungs collapses because of heaviness of mucus)
hemoptysis (spitting out blood)
R sided heart failure
many other systems involvement
Pulmonary exacerbation in cystic fibrosis
* progressive decline of lung function
* Increase cough and sputum production (or change in what you’re actaully expelling)
* fever, missing school
* weight loss
* increased RR
* decreased EX tolerance
* decreased FEV1 of 10% within 3 months
* Hemoglobin saturation decrease of 10% within past 3 months
* New findings infulatrates on chest X-ray will indicate an exacerbation
Medical amangement of cystic fibrosis (remember mucus is so thick and sticky the cilia cant push it out of your lungs)
* DX: genetic screen during pregnancy, screen at birth, sweat test, FEV1 and FVC, pancreatic insufficiency CF-releated diabetes mulitis, bone mineral density
Avoid trendelenburg positioning in treatment for all ages (this is head down)
* modified postural drainage
Airway clearance - chest therapy
Breathing EX
Higher frequency chest wal oscillation vest - viborates and breaks down mucus so its easy to expell
Prescribed exercise program
Cystic fibrosis
Hereditary disease resulting in viscous secretions
* High risk of infection (on antibiotic)
Pharmacaological management: maintain airway patency
bronchodilators and mucolytic and/or expectorant drugs - works on decreasing that mucus production and expelling it out
Systemic glucocorticoids
* to work on reoccuring inflamation
NSAIDs
* inflamation
Anti-infectious agents also play a key role in the treatment of cystic fibrosis, and respiratory infections are treated with appropriate antibiotic agents
* Azithromycin - very common antibiotic for infections in CF
A patient with COPD suddently reports nausea, confusion, and irritability. Which of the following drugs should you particulary be cautious of
a) Xanthine deriviatives
b) Leukotrienes
c) Cromones
d) Bronchodilators
a
quiz review 1:25:00
