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Pharma 2 > Lecture 8: Obstructive Lung Disease > Flashcards

Lecture 8: Obstructive Lung Disease Flashcards

1
Q

What is obstructive lung disease

A

Can’t get air out

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2
Q

What is restrictive lung disease?

A

Can’t get air in

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3
Q

Most common obstructive lung disease

A

COPD (often used as an umbrella term)

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4
Q

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

A
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5
Q

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

A
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6
Q

Chronic bronchititis is hypesecrtion of mucus in the bronchus

A
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7
Q

What are the different obstructive pulmonary diseases

A

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

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8
Q

What 3 things does Spirometry consist of (3)

A

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

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9
Q

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

A

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

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10
Q

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

Risk factors (2)

GOLD Guidelines

A

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+

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11
Q

GOLD standards are what

A

what to do for COPD

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12
Q

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

A
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13
Q

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

A
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14
Q

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

A
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15
Q

Dyspnea scale

A
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16
Q

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

A
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17
Q

How to help a patient quit smoking

A
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18
Q

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

A
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19
Q

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

A
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20
Q

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

A

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

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21
Q

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

A

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

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22
Q

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

A
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23
Q

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

Why are the perfurfed

MOA

A

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.

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24
Q

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

A

Anticholinergics

so the decrease those bronchospasms

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25
Q

Most common anticholinergics

A

Spiriva

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26
Q

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

A
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27
Q

Side effects w/ anticholinergics (6)

A

Due to CNS activation

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

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28
Q

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

A

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

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29
Q

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

A

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

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30
Q

Xanthine Derivative Bronchodilators

A
31
Q

What do zanthine derivatives end in?

A

lline

32
Q

z

These are steriods
* mostly one

have to be careful using these because they are glucosteriods which increase glucose - bad w/ diabetes

A
33
Q

COPD has mucus + bronchosmpasms
* we need to preven these

GOAL for treating: Maintaining airway patency and preventing airflow restriction

A
34
Q

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

A
35
Q

Long acting beta adergenc (LABA)

LAMA

in combination

mild
* LABA+LAMA
* or just bronchodilator

gold classification

A
36
Q

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

A
37
Q

Be able to dilinate long acting and short acting inhaled bronchodilators

Inhaled corticosteriods is list from earlier

A
38
Q

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

A

Beta-adergenics is the answer
* Increases bronchodilation

Antitussives: used to reduce cough

Antihistamines: For inflammation / immune response / allergies

Mucolytics: break up mucus

39
Q

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

A

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

40
Q

Clinical manifestation of asthma (4)

A

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

41
Q
A
42
Q

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

A
43
Q

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

A
44
Q

Adverse effects of glucocorticoids

A

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

45
Q

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

A
46
Q

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

LABA = ol

A
47
Q

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

A

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

48
Q

Cromones side effects

A

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

49
Q

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

A

4

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

50
Q

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

A

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

51
Q
A
52
Q

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

A

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)

53
Q

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)

A
54
Q

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

A

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

55
Q

Three types of emphysema
* most common

A

Centrilobular - most common - affects the upper growths
Panlobular
Pariseptal

56
Q

What happens to the alveoli walls w/ emphasima

A

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

57
Q

Clinical manifestation w/ emphysema (5)

Treatment (5)

A

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)

58
Q

Smoking is a major compoenent of both

A
59
Q

This is the barrel chest look w/ emphysema

notice the white cloudy look

A
60
Q
A
61
Q

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

A

D

Smoking is one, but genetic is leading cause

62
Q

Exercise-Induced bronchospasm or bronchoconstriction

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

A

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

63
Q

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)

A

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

64
Q

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%

A
65
Q

Inherited disorder of ion transportation (sodium and calcium) in exocrine glands
* what systems involved

Do they develop obstructive or restrictive lung disease?

pathogensis?

A

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)

66
Q

Where does cystic fibrosis primarily affect the lungs?

A

Bronchioles

67
Q

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

A
68
Q

Early stages of cystic fibrosis
* how does cough start?

A

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

69
Q

Advanced stage cystic fibrosis

A

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

70
Q

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

A
71
Q

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

A
72
Q

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
73
Q

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

a

74
Q

quiz review 1:25:00

A

Pharma 2 (20 decks)

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