Lecture 8: Obstructive Lung Disease

Question 1

What is obstructive lung disease

Answer 1

Can’t get air out

Question 2

What is restrictive lung disease?

Answer 2

Can’t get air in

Question 3

Most common obstructive lung disease

Answer 3

COPD (often used as an umbrella term)

Question 4

KNOW: For asthma you have increased mucus where the broncioles are
* mostly classified as obstructuive

Question 5

In emphysema its hard to get their air out because the alveoli are going to collapse and trap gas inside

Question 6

Chronic bronchititis is hypesecrtion of mucus in the bronchus

Question 7

What are the different obstructive pulmonary diseases

Answer 7

A - Asthma
B - Bronchiectasis
C - Cystic Fibrosis/Chronic Bronchitis
D - Decreased FEV1/FVC ratio
E - Emphysema

Question 8

What 3 things does Spirometry consist of (3)

Answer 8

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

Question 9

What is a normal FEV1/FVC ratio?
* also FEV1 and FVC have to be above __ of perdicted value

Answer 9

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

Question 10

What are the 4 clinical manifestations of chronic obstructive pulmonary disease (COPD)

Risk factors (2)

GOLD Guidelines

Answer 10

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+

Question 11

GOLD standards are what

Answer 11

what to do for COPD

Question 12

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

Answer 12

Question 13

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

Question 14

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

Question 15

Dyspnea scale

Question 16

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

Question 17

How to help a patient quit smoking

Question 18

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

Question 19

KNOW: The underlying cause of COPD is not treated
* However, the medications are aimed at treating the symptoms - which is airway obstruction

Question 20

Why do we use beta adergenic drugs for COPD?
* What kind of beta blockers
* What 4 drugs are this?

Answer 20

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

Question 21

Adverse effects of Beta-Adergenic drugs for COPD (3)

Answer 21

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

Question 22

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

Question 23

Inflammatory compounds that are especially important in mediating the airway inflammation that underlies bronchoconstrictive disease

Why are the perfurfed

MOA

Answer 23

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.

Question 24

What drugs block muscarinic cholinergic receptors and prevent acetylcholine induced bronchoconstriction, thus improing airflow in certain types of bronchospastic disease

Answer 24

Anticholinergics

so the decrease those bronchospasms

Question 25

Most common anticholinergics

Answer 25

Spiriva

Question 26

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

Question 27

Side effects w/ anticholinergics (6)

Answer 27

Due to CNS activation 1) dry mouth 2) Constipation 3) Urinary retention 4) Tachycardia 5) Blurred vision 6) Confusion

Question 28

What do Xanthine Derivatives do? * MOA * Why cant you take these for long

Answer 28

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

Question 29

Recommended levels for xanthine derivatives * what is the most serious limitation in the use of these

Answer 29

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

Question 30

Xanthine Derivative Bronchodilators

Question 31

What do zanthine derivatives end in?

Answer 31

lline

Question 32

# z These are steriods * mostly one have to be careful using these because they are glucosteriods which increase glucose - bad w/ diabetes

Question 33

COPD has mucus + bronchosmpasms * we need to preven these GOAL for treating: Maintaining airway patency and preventing airflow restriction

Question 34

KNOW theophylline is used for COPD but is a xanthine deriviative (so have to be careful)

Question 35

Long acting beta adergenc (LABA) LAMA in combination mild * LABA+LAMA * or just bronchodilator | gold classification

Answer 35

Question 36

First thing to look at with inhalers is to look at how theyre administering it * ejucate there

Question 37

Be able to dilinate long acting and short acting inhaled bronchodilators Inhaled corticosteriods is list from earlier

Question 38

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

Answer 38

Beta-adergenics is the answer * Increases bronchodilation Antitussives: used to reduce cough Antihistamines: For inflammation / immune response / allergies Mucolytics: break up mucus

Question 39

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

Answer 39

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

Question 40

Clinical manifestation of asthma (4)

Answer 40

1) Wheezing cough 2) Dry or productive sputum with plugs (mucus getting stuck --> leads to infection) 3) Anxiety 4) Decreased chest wall symmetry

Question 41

Question 42

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

Question 43

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

Question 44

Adverse effects of glucocorticoids

Answer 44

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

Question 45

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

Question 46

anti inflamatory steriod combination in combination with long acting beta 2 bronchodilator (management of asthma) * Advair * Symbicort * dulera * all very common LABA = ol

Question 47

When do you use cromones for asthma? * what do they do * What do they do to mast cells?

Answer 47

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

Question 48

Cromones side effects

Answer 48

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

Question 49

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

Answer 49

4 this is why you have to be careful if they have diabetes

Question 50

Obstructive, restrictive disorder; permanent dilation of airways that have a normal diameter of greter than 2 mm * etilogy * pathogensis

Answer 50

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

Question 51

Question 52

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

Answer 52

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)

Question 53

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)

Question 54

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

Answer 54

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

Question 55

Three types of emphysema * most common

Answer 55

Centrilobular - most common - affects the upper growths Panlobular Pariseptal

Question 56

What happens to the alveoli walls w/ emphasima

Answer 56

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

Question 57

Clinical manifestation w/ emphysema (5) Treatment (5)

Answer 57

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)

Question 58

Smoking is a major compoenent of both

Question 59

This is the barrel chest look w/ emphysema notice the white cloudy look

Question 60

Question 61

What is the leading risk factor for emphysema 1) Prolonged steriod use 2) Smoking 3) Respiratory failure 4) Genetic Origin

Answer 61

D Smoking is one, but genetic is leading cause

Question 62

Exercise-Induced bronchospasm or bronchoconstriction Acute, reversible airway obstruction that occurs 5-15 minutes after vigorous exercise * risk factors * etiology * Symptoms * treatment

Answer 62

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

Question 63

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)

Answer 63

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

Question 64

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%

Question 65

Inherited disorder of ion transportation (sodium and calcium) in exocrine glands * what systems involved Do they develop obstructive or restrictive lung disease? pathogensis?

Answer 65

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)

Question 66

Where does cystic fibrosis primarily affect the lungs?

Answer 66

Bronchioles

Question 67

KNOW: w/ cycstic fibrosis both parents must be carries of the defective gene

Question 68

Early stages of cystic fibrosis * how does cough start?

Answer 68

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

Question 69

Advanced stage cystic fibrosis

Answer 69

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

Question 70

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

Question 71

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

Question 72

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

Question 73

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

Answer 73

a

Question 74

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