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Patho 1 (PATH 254) > Module 2 COPD > Flashcards

Module 2 COPD Flashcards

1
Q

LAMA

A

Long acting controller for smooth muscle relaxation and dilation.

  • Slower onset w/long duration
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2
Q

Is tiotropium a LAMA or SAMA?

A

LAMA

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3
Q

COPD is largely caused by smoking; according to GOLD what is the more definitive cause?

A

Complex mix of genes and environment

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4
Q

COPD symptoms

A

SOB

Chronic cough

Sputum

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5
Q

Risk factors for COPD

A

Host Factors, but generally:

  • Tobacco
  • Occupation
  • In/outdoor pollution
  • Genetic predisposition
  • COPD increases with age
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6
Q

How do you test/diagnosis COPD?

A

Spirometers

(FEV1/FVC)

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7
Q

COPD is formally diagnosed via spirometers to test post-bronchodilator. FEV1/ FVC ratio.

what ratio would be consistent with COPD?

A

FEV1/ FVC ratio less than 0.70

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8
Q

Add slides on patient history

edit

A
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9
Q

How is Spirometry used as a tool to diagnose COPD?

aka how does it work?

A

Objectively measures airflow limits

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10
Q

What does normal vs obstructed airflow look like?

A
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11
Q

Is COPD a obstructive or restrictive disease?

A

obstructive

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12
Q

What is the difference between obstructive and restrictive lung diseases?

A

obstructive: make it hard to exhale air out of the lungs.

Restrictive: makes it hard to expand their lungs with air.

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13
Q

What are 2 pathologies that make up COPD

A

Chronic bronchitis and emphysema

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14
Q

What is dynamic compression?

A

Premature compression of airways.

(leading to increased airway resistance)

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15
Q

What could cause increased airway resistance in a COPD patient

A

Air trapping

Increased secretions

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16
Q

What direction does the equal pressure point (EPP) move in COPD?

A

Toward the alveoli into the non-cartilaginous airways.

Palv < Ppl

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17
Q

Common symptoms of COPD

A

Persistent cough

Increased mucous production

Dyspnea

Muscle fatigue

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18
Q

Hallmark sign of COPD

A

productive cough

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19
Q

Panlobular emphysema

A

Type of emphysema involving distention and destruction of the entire primary respiratory lobule

  • usually associated with 1-antitrypsin deficiency
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20
Q

Centrilobular emphysema

A

Weakening and enlargement of respiratory bronchioles in the proximal portion of acinus.

  • Associated with smoking.
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21
Q

What criteria would classify as Chronic bronchitis?

A

presence of cough and sputum production for at least 3 months in 2 consecutive years

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22
Q

What does emphysema cause?

A
  • Oxidative stress
  • Airway remodeling
  • enzyme; enzyme inhibitor imbalance.
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23
Q

Symptoms to consider a diagnosis for COPD?

A
  • dyspnea
  • recurrent lower resp. tract infection
  • chronic cough/sputum
  • history of risk factors
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24
Q

GOLD diagnosis of COPD

A

FEV1/ FVC ratio < 0.70

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25
Q

How often is spirometry done for COPD

A

q6months to 1yr

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26
Q

GOLD 1 airflow limitation

A

FEV1 > 80% predicted

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27
Q

GOLD 2 airflow limitation

A

FEV1 50-80% of predicted

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28
Q

GOLD 3 airflow limitation

A

FEV1 30-50% predicted

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29
Q

GOLD 4 airflow limitation

A

FEV < 30% of predicted

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30
Q

mMRC grade 0

A

I only get breathless with strenuous exercise

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31
Q

mMRC grade 2

A

I walk slower than people of the same age on the level because of the breathlessness, or I have to stop for breath when walking on my own pace on the level.

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32
Q

mMRC grade 3

A

I stop for breath after walking about 100 meters or after a few minutes on the level

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33
Q

mMRC grade 4

A

I am too breathless to leave the house or I am breathless when dressing or undressing

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34
Q

Mild exacerbation treatment (Tx)

A

Only with Short acting bronchodilator agent (SABA)

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35
Q

Moderate COPD exacerbation Tx

A

SABA plus oral antibiotics or oral corticosteroids (OCS)

  • OCS like prednisone or methylprednisolone
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36
Q

What are the benefit of oral corticosteroids in COPD?

A
  • Help to improve lung function
  • Improves oxygenation
  • Reduces recovery time
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37
Q

Severe exacerbation Tx

A

Hospitalization with or without resp. failure may need NIV (very beneficial), intubation/ventilation

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38
Q

True or False: A pt who has had a COPD exacerbation in the past is at an increased risk for future exacerbations.

A

True.

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39
Q

Benefits of long-term supplemental oxygen therapy (LTOT)

A

Helps improve survival benefit

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40
Q

Indications for long-term supplemental oxygen therapy (LTOT)

A

Needs to have restive PaO2 < 55mmHg or <60mmHg with either cor pulmonale, edema, erythrocytosis, polycythemia

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41
Q

Pre-ganglionic receptors on the sympathetic system are comprised of?

A

Nicotinic receptors
(cholinergic receptors that release acetylcholine)

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42
Q

A COPD patient with a eosinophil count of 25/uL and prescribed a LABA with infrequent AECOPD continues to have dyspneic episodes:

A

Should be prescribed a LAMA

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43
Q

Increased airway resistance is a contributing factor to which disease process?

A

obstructive

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44
Q

What is Panacinar emphysema?

A

Involves all portions of the acinus and secondary pulmonary lobule more or less uniformly.

  • It predominates in the lower lobes and is the form of emphysema associated with 1-antitrypsin deficiency.
  • TLDR; worsens the in the lower lobes aka alveoli!!!
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45
Q

What does acetylcholine do to airways?

A

Regulates bronchoconstriction and mucus secretion

  • includes inflammation and regulation of airways
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46
Q

What do anticholinergic drugs do?

A

Block the activity of neurotransmitter acetylcholine (Ach) at both central and peripheral nervous system synapses, reducing PNS acitivty which affects the organs differently/

  • Lungs vasodilate by preventing bronchoconstriction
  • Increases HR by blocking vagal tone
  • GI reduces contractions for cramps
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47
Q

What are adrenergic drugs used for?

A

Adrenergic agonists that bind to alpha and beta receptors that depending on the receptor site affects:

  • local vasoconstriction (for hypotension/shock)
  • Relaxes (bronchodilates) (b2) or constricts smooth muscles (a1)
  • relief of allergic states (anaphylaxis included)
  • Increase HR
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48
Q

Generally, what do B1 and B2 receptors do?

A

B1 = excite

B2 = relax

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49
Q

Group A Combined assesment

A

low risk low symptoms
GOLD 1 or 2

mild to moderate airflow limitation
0-1 exacerbations per year
mMRC 0-1
CAT <10

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50
Q

Group B combined assessment

A

low risk more symptoms
GOLD 1 or 2

mild to moderate airflow limitations
0-1 exacerbations per year
mMRC 2-4
CAT > 10

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51
Q

Group C combined assessment

A

High risk less symptoms
GOLD 3 or 4

Severe to very severe airflow limitations
>2 exacerbations/yr
mMRC 0-1
CAT <10

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52
Q

Group D combined assessment

A

High risk more symptoms
GOLD 3 or 4

Severe or very severe airflow limitation
>2 exacerbations per year
CAT > 10

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53
Q

Group A treatment

A

Short acting bronchodilator (SABA)

Salbutamol or ipatropium

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54
Q

Group B treatment

A

LAMA or LABA

Salmeterol or Tiotropium

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55
Q

Group C treatment

A

LAMA or LAMA/LABA

  • Add ICS to either of these if eosinophil count is > 300
  • (or less than 100 after hospitalization)
  • triple therapy (all 3)
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56
Q

Why would ICS not work well on COPD?

A

COPD has neutrophillic inflammation as opposed to eosinophilic inflammation (asthma related).

Tobacco smoke also decreases effiacy bc:

  • Has an immunosuppressive effect on lungs
  • Alters lungs response via neutrophil activity and oxidative sterss
  • Increase glucocrticoid resistance (less respsonsive)
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57
Q

When to add PDE4 inhibitor

A

when eosinphil levels are < 100 and triple therapy is not effective

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58
Q

What can chronic inflammation result in?

A

small airway diseases

chronic bronchitis

destruction of lung parenchyma tissue

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59
Q

What is the pathophysiology of COPD?

A

Loss of elastic recoil and airway attachment

Leading to…
-> airways collapse during expiration
->Decreased surface area available for gas exchange

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60
Q

What is emphysema

A

Destruction of alveoli surface area

  • usually due to harmful substances like cigaratte smoke
  • leads to loss in elastic fibres = less recoil
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61
Q

What are 2 types of emphysema?

A

Panlobular

centrilobular

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62
Q

Define panlobular emphysema

A

Abnormal weakening and enlargement of all air spaces distal to terminal bronchioles

  • aka primarily affects the alveoli
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63
Q

Define centrilobular emphysema

A

abnormal weakening and enlargment of resp. bronchioles and alveoli in proximal portion of acinus

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64
Q

What genetic component could cause someone to develop COPD

A

Alpha 1 anti trypsin deficiency

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65
Q

What is the goal of COPD treatment?

A

Take away what is causing the lung damage

i.e tobacco cessation

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66
Q

What are the goals of treatment for stable COPD?

A

Reduce symptoms

reduce risk; prevent and treat exacerbations

reduce mortality

prevent disease progression

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67
Q

What interventions are shown to decrease mortality in COPD pts w/resting hypoxemia?

A

tobacco cessation and O2 therapy

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68
Q

what should not be a guiding factor in treatment of COPD?

A

severity of airflow limitation

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69
Q

What parts assist w/reducing symptoms in COPD?

A

relieve symptoms

improved exercise tolerance

improve health status

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70
Q

What are the intial pharm treatments for groups
i.e ABCD?

A

A -> bronchodilators

B -> LABA (or LAMA’s)

C -> LAMA

D -> LAMAs or [LAMA/LABA] or [ICS + LABA]

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71
Q

For pt’s w/persistent long acting bronchodilator therapy, what is recommended?

A

Escalation to:
-LABA
-LAMA
-[LABA/ICS]

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72
Q

What predicts a low likelihood of beneficial ICS response

A

Blood eosinophil count < 100 cells/Ul

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73
Q

What can be done for pt who develops further exacerbations while on LABA/LAMA?

A

Escalation to triple therapy (LABA/LAMA/ICS)

  • addition w/PDE4 inhibitor
  • addition of antibiotics (azithromycin)
  • w/assumption than eosinophil < 100
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74
Q

What COPD pt’s receive ICS?

A

Those w/High risk of exacerbation

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75
Q

What COPD pt should have Pulmonary rehab (PR)?

A

Any that had a AECOPD should take part in PR w/1 month of AECOPD

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76
Q

What is pulmonary rehab [PR]?

A

Standard of care for COPD pt w/symtpoms despite optimal pharm therapy.

Improves:

  • quality of life
  • Dyspnea
  • healthcare utilization
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77
Q

What is AECOPD?

A

Defined by gold as:

Acute worsening of resp. symptoms that result in requirement for additional therapy

78
Q

What is the most common causes of COPD exacerbations?

A

Respiratory tract infections

79
Q

What can prevent/treat exacerbations

A
  • Antibiotics (when indicated) q5-7d
  • NIV
80
Q

Treatment for mild exacerbations classes?

A

SABA

81
Q

Treatment for moderate exacerbations classes?

A

SABA w/antibiotics

82
Q

Treatment for severe exacerbations classes?

A

Hospital

typically acute resp. failure

83
Q

how long do AECOPD symptoms normally last?

A

7-10 days (sometimes longer)

84
Q

What are AECOPD management options?

A

Inhaled bronchodilators

PO antibiotics for sputum w/systemic corticosteroids
-goal is to keep SaO2 > 90%

NIV for hypercapnia
-pH < 7.3

85
Q

What is the success rate for NIV treatment?

A

80-85%

86
Q

Indications for invasive ventilation in AECOPD?

A

unable to tolerate NIV

Post resp/cardiac arrest

decrease LOC

Aspiration

hemodynamic instability

87
Q

Why do we avoid invasive ventilation?

A

greater morbidity risk and increased length of hospital stay

88
Q

how can we reduce COPD progression?

A

smoking cessation

long term O2 therapy

lung transplant

annual flu vaccines

89
Q

indications for O2 therapy?

A

resting PaO2 < 55

SaO2 < 88
PaO2 <55

sleep; same with associated complications like pulmonary hypertension and cardiac arrhythmias

90
Q

What are some surgical interventiosn for end stage copd

A

lung transpant
lung vol reduction surgery

pt with aat deficency = intravenous with purified aat from human blood donor

91
Q

What do bronchodilators do?

A

help reduce dyspnea

improve lung function

92
Q

2 main classes of bronchodilators?

A

Beta 2 agonists

anti-muscarinics

93
Q

What do antimuscarinic agents do?

A

Block the action of acetylcholine on receptors

->leads to bronchodilation and symptom reduction

94
Q

Where are beta 2 receptors found?

A

bronchial and vascular smooth muscles

95
Q

When is anti IGE therapy used?

A

for asthma that bypasses standard treatments.

usually in youth w/continued uncontrolled ashtma and allergies

96
Q

3 commons LAMAs?
(actual drug names)

A
  • Tiotropium (spirvia)
  • Aclidnium Bromide (Tudorza)
  • Glycopyronnium Bromide (Seebri)
97
Q

What are 3 LABAs?
(actual drug names)

A

-Formoterol (oxeze)

-Salmeterol (serevent)

-Indacterol (Onbrez)

98
Q

What are the differences between SABAs and LABAs?

A

long acting continuously keeps airways open
-sees long term use

shorting acting = emergencies
-“rescue inhalers”

99
Q

What are the adrenergic receptors

A

Alpha and beta sympathetic receptors

100
Q

What kind of receptors are the alpha and beta receptors?

A

g-coupled receptors

101
Q

General innervation of Alpha 2 receptors result in what?

A

inhibitory response

102
Q

Activation of alpha 1 receptors illicit what response?

A

sympathetic

Typical contractions

103
Q

Norepinephrine is released by?

A

All postganglionic neurons of the sympathetic nervous system except those that stimulate sweat glands

104
Q

Acetylcholine (AcH) stimulates what on sympathetic and parasympathetic postganglionic neurons at the neuromuscular junction?

A

nicotinic receptors

105
Q

Norepi stimulates what on tissues innervated by sympathetic POSTganglionic neurons?

A

alpha and beta receptors

106
Q

What are the parasympathetic receptors?

A

muscarinic and nicotinic

107
Q

what degrades AcH?

A

cholinesterase

108
Q

sympatholytic vs sympathomimetic drug?

A

mimetic = mimics effects of the sympathetic nervous system (SNS).

  • elevated HR and sweating etc.

lytic = works against SNS

  • used when someones heart is beating too fast
  • used for high blood pressure
  • i.e beta blockers
109
Q

Examples of alpha agonists?

A

norepinephrine
epinephrine
dopamine (high doses)

110
Q

Generally alpha (mostly a1) serve which function?

A

regulate vascular smooth muscle tone

(think peripheral vasculature)

111
Q

mMRC is a scale that measures…

A

Dyspnea; via questions

112
Q

mMRC grade 1

A

I get SOB when hurrying on the level or walking up a slight hill

113
Q

For pts w/persistent exacerbations on LABA, what is the next step?

A

Escalation to:
-[LABA/LAMA]
-[LABA/ICS] is

114
Q

When would a [LABA/ICS] combo be preferred?

A

For patients with ONE exacerbation per year, an eosinophil count >300/uL identifies a patient more likely to respond to LABA/ICS treatment

For patients with TWO exacerbations per year or one exacerbation leading to hospitalization LABA/ICS treatment can be considered at eosinophil counts >100 cells/uL

115
Q

The most common cause of exacerbations are

A

Respiratory tract infections; normally triggered via bacterial infections and environmental factors (pollution)

116
Q

Why would you use a SABD for a exacerbation rather than a LAMA?

A

Faster onset

117
Q

What can improve lung function (FEV1), oxygenation, and shorten recovery time (and hospital duration)?

A

Systemic corticosteroids (no longer than 5-7 days of therapy)

-systemic corticosteroids are typically not good for you.

118
Q

When would you prescribe a pt w/antibiotics?

A

Only w/a positive test of a bacterial infection

119
Q

Which mode should be used in COPD pts w/acute resp. failure who have no absolute contraindications?

A

NIV

120
Q

What are the benefits of NIV?

A

Improves gas exchange

reduce WOB

Reduce stress need needed for intubation

decreases hospital duration

Improves survival

121
Q

what can predict future AECOPD events?

A

Past AECOPD

122
Q

What is a requirement of NIV

A

spontaneously awake conscious patient because they need to be able to keep their air way open (Prevent aspiration)

123
Q

CPAP/BIPAP: For positive pressure stents airways open, What does the difference between IPAP and EPAP do ?

A

Provides Pressure support; Augments their Vt

-helps transfer the support of the machine to improve their MV

124
Q

Tx for mild COPD exacerbations

A

Treated w/SABDs

125
Q

Tx for moderate COPD exacerbations

A

Treated with SABD, antibiotics, and/or oral corticosteroids.

126
Q

Tx for Severe COPD exacerbations

A

Require hospital; severe are usually associated w/acute resp. failure

127
Q

If NIV fails, what are the next steps?

A

intubation and mechanical ventilation

128
Q

AECOPD Management Progessive plan

A

-Inhaled bronchodilators; beta 2 agonist in particular PRN

-oral antibiotics if purulent sputum is present (5-7d)

-Short course of systemic corticosteroids (5-7d)

-supplemental oxygenation to keep SaO2 > 90

-w/hypercapnia (pH < 7.3); NIV
-pay attention to 7.28

129
Q

AECOPD: what indicator would you prescribe antibiotics?

A

presence of purulent sputum

130
Q

AECOPD Management ventilation; Why do you use NIV vs invasive ventilation?

A

Shown to improve oxygenation and improve resp. acidosis w/o risk of vent. acquired pneumonia

-NIV can be discontinued w/o weening period

-NIV decreases RR, WOB, and severity of breathlessness

131
Q

Indications for invasive ventilation?

A

Unable to handle/use to tolerate NIV

post resp. or cardiac arrest

decreased LOC

Massive aspiration/vomiting

Severe hemodynamics instability
-can reduce venous return

Life threatening hypoxemia

132
Q

Reducing progression of COPD; how can you enhance survival?

A

-Smoking cessation is the first line of intervention

-Long term oxygen therapy (LTOT)

annual influenza and pneumoccal vaccinations

-some end stage may also benefit from a lung transplant or lung volume reduction surgery

133
Q

Indications for long term oxygen therapy (LTOT)

A

Continuous O2;
-resting PaO2 < 55 mmHg

SaO2 @ 89% and resting PaO2 56-59 mmHg in the presence of:
-> dependant edema; suggests CHF
-> P. polmonale on the ECG (sharp peaked P waves)
-> Erythrocytosis (hematocrit > 56%)

Non continuous O2

134
Q

SaO2 @ 89% and resting PaO2 56-59 mmHg in the presence of: what does the presence of depedant edema suggest?

A

CHF

135
Q

Indications for long term O2 therapy (LTOT); what does non continuous O2 entail?

edit
slide 15 of COPD management

A

Associated with flow rate of O2 and hours per day due to factors such as exercise or exertion.

-Exercise;
PaO2 <55 or SaO2 < 88 w/low level of exertion

-During sleep; (save values as above) w/complications such as pul. hypertension, daytime sommlence or cardiac arrhythmias

136
Q

What are surgical interventions for end stage COPD?

A

lung transplant

lung volume reduction surgery (LVRS)

137
Q

For pts w/AAT deficiency and COPD what are additional therapies?

A

intravenous augmentation w/purified preparation of AAT from human blood donors is recommended

138
Q

What is the most common situation to step down from a COPD medication may be considered?

A

when there is no improvement to dyspnea or exercise tolerance in stable COPD patients

139
Q

What is the best intervention and general advice for a patient recently diagnosed w/mild COPD which could improve their symptoms and possibly increase their survival?

A

Tobacco cessation

140
Q

What are signs of upper airway obstruction?

A
  • Stridor
  • Dyspnea
  • drooling
141
Q

When would a lobe resection be performed?

A

For patients w/severe COPD

142
Q

How does a lobe resection benefit patients w/severe COPD?

A

Increases surface area between alveoli and pulmonary capillaries

143
Q

Airway remodeling is a characteristic change associated w/chronic bronchitis. What is usually associated w/bronchitis?

A

Increased mucous viscosity and secretion

AND

reduction in elastic protiens of the lung parenchyma

144
Q

Pathobiology of COPD

A

Impaired lung growth

Lung injury

Lung and systemic inflammation
-oxidative stress
-airway remodelling
-hypersecretion of mucus

145
Q

Generally describe Empysema

A

Destruction and damage to alveoli decreasing alveolar surface area

146
Q

What is panlobular empysema

A

Abnormal weakening/destruction and enlargement of alveoli distal to the acinus

147
Q

What is centrilobular emphysema?

A

Weakening/destruction and enlargement of the alveoli near the bronchioles

more associated w/smoking

148
Q

what symptoms are the common to find w/COPD?

A

Productive cough

Weakening of the distal airways

chronic limitation of airflow

air trapping and hyper inflammation

destruction of the lung parenchyma, including alveolar-capillary membrane.

149
Q

Chronic Bronchitis is defined as?

A

THe presence of a productive cough foratleast 3 months in 2 years

150
Q

Etiology of chronic bronchitis

A

typically from smoking

exposure to air pollution

irritants

151
Q

Goals of treatment for COPD

A

Focus on tobaccos cessation; it can delay the progression of disease but lung damage is permanent

152
Q

If a pt has a predicted FEV1 >80* their GOLD airway limitation severity would be classified as

A

mild

153
Q

If a pt has a predicted FEV1 between 30-50% their GOLD airway limitation severity would be classified as

A

Severe

154
Q

If a pt has a predicted FEV1 between 50-79% their GOLD airway limitation severity would be classified as

A

Moderate

155
Q

If a pt has a predicted FEV1 < 30% their GOLD airway limitation severity would be classified as

A

Very severe

156
Q

A pt only gets breathless w/strenuous exercise, what is his mMRC grade?

A

Grade o

157
Q

A pt gets SOB when hurting on the level or walking up a slight hill. What is their mMRC grade?

A

Grade 1

158
Q

A pt walks slower than people of the same age on the level because of breathlessness, or has to stop for a breath when walking on their own pace. What is their mMRC grade?

A

Grade 2

159
Q

A pt has to stop for breath after walking about 100 enters or after a few mins on the level. What is their mMRC grade?

A

Grade 3

160
Q

A pt is too breathless to leave the house or breathless when dressing/undressing. What is their mMRC?

A

Grade 4

161
Q

mMRC evaluates what?

A

perception of dyspnea w/activity

162
Q

How long do COPD exacerbation symptoms usually last?

A

7-10 days

163
Q

Persistent dyspnea and SOB are strongly associated with what?

A

increased risk of exacerbation

164
Q

What are the recommended initial bronchodilators to treat AECOPD?

A

SABA

with or w/o SAMA

165
Q

What are 5 ways to help manage AECOPD?

A

Bronchodilators (SABA and SAMA)

Antibiotics if purulent sputum is present

systemic corticosteroids

supplemental oxygen

NIV if pH =<7.3

166
Q

What are the recommended diesels for salbutamol for a MDI?

A

100 mcg + 2 puffs inhaled every 4 hours with a spacer

but really; 2 puffs q1h

167
Q

What is the indication for long-term oxygen therapy?

A

Resting PaO2 of =< 55 mHg.

Alt.
SaO2 <88 during exercise.

168
Q

What are some interventions for pt’s w/end stage?

A

Lung transplant

Lung volume reduction surgery (LVRS)

169
Q

Lobe resections are an effective intervention for severe COPD pts. how does a lobe resection benefit these pts?

A

Increases surface area between alveoli and pulmonary capillaries

170
Q

What is a complication of AAT deficiency?

A

Can cause emphysema
-> increasing pulmonary compliance (loss of elastic property)

171
Q

Problems w/oxidative stress?

A

Breakdowns proteins and all involved enzymes (and inhibitors)
->parenchyma reduced
->causes imbalances

172
Q

Steps for reducing progression of COPD

(enhancing survival)

A
  1. Smoking cessation
  2. Long-term oxygen therapy (LTOT)
  3. Annual influenza and pneumococcal vaccinations
  4. lung transplant
173
Q

which groups of the combined COPD assessment suggest a high risk of symptoms?

A

C and D

however
1 or more hospital visits for COPD exacerbations are always high risk

174
Q

How does smoking cessation help reduce the progression of COPD?

A

Slows rate of FEV1 decline to same age smokers

175
Q

GOLD risk classification A

A

Low risk ; less symptoms

Gold 1 or Gold 2
mild to mod airflow limitations

and/or
mMRC grade 0-1
CAT < 10

176
Q

GOLD risk classification Ç

A

High Risk; less symptoms

Gold 3 or 4
severe -> very severe airflow limitation

and/or
>2 exacerbations year
mMRC grade 0-1
CAT score < 10

177
Q

GOLD risk classification B

A

Low risk ; more symptoms

Gold 1 or Gold 2
mild to mod airflow limitations

and/or

0-1 exacerbation/year
mMRC grade > 2
CAT > 10

178
Q

GOLD risk classification D

A

High Risk - More symptoms

Gold 3 or Gold 4
Severe or very severe Airflow limitations

and/or

> 2 exacerbations/year
mMRC grade > 2
CAT > 10

179
Q

AECOPD management; Indicators to transition from NIV to invasive?

A
  • Unable to tolerate NIV
  • Post resp. or cardiac arrest
  • Decreased LOC
  • Massive aspiration/persistent vomiting
  • severe hemodynamics instability
  • life-threatening hypoxia
180
Q

Group D treatment

A

LAMA or LAMA/LABA

Add ICS to either of these (LABA/ICS or triple therapy)
if eosinophil count is >300 or >100w/recent hospitalizations

181
Q

When does ICS not work well on COPD?

A

Tobacco smoke downplays the ICS action

182
Q

What conditions like asthma, COPD, or those associate w/chronic bronchitis, what are typical structural changes?

(5)

A
  1. Chronic inflammation of the wall of peripheral airways
  2. excessive mucous production and acclamation
  3. parietal/total mucous plugging of airways
  4. smooth muscle constriction of bronchial airways (bronchospasm)
  5. air trapping and inflation of alveoli
183
Q

Emphysema is characterized by what?

A

The weakening and permeant enlargement of air spaces distal to the terminal bronchioles; and by does turn on of the alveolar walls

-decreased SA for gas exchange
-collapse of expiration in response to increased intrapleural pressures

184
Q

What are the alternative names for panlobular and centrilobular emphysema

A

Panacinar and centriacinar emphysema

185
Q

Centriacinar emphysema involves which portion of the resp. system and alt name?

A

proximal portion of the acinus.

alt. name = centrilobular

186
Q

Panacinar emphysema is involves which part of the resp. system and alt. name?

A

enlargement of alveoli distal to terminal bronchioles

panlobular

187
Q

which type of emphysema is associated w/smoking?

A

centriacinar (centrilobular)

188
Q

Difference between centrilobular and panlobular emphysema

A
189
Q

which type of emphysema is most severe?

A

centrilobular

190
Q

COPD is typically characterized by what?

A

Persistent airflow limitation

It is progressive and not fully reversible

191
Q

Obstructive breathing pattern will do what to minimize WOB?

A

Minimize their WOB.

  • slow down RR allows for long exhales
192
Q

Oral corticosteroids vs inhaled corticosteroids?

A

Both improve dyspnea

  • OCS are used primarily for flare ups
  • ICS more for long term use, to prevent flare ups and make receptors available for bronchodilators

Patho 1 (PATH 254) (18 decks)

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