L10 COPD Flashcards

1
Q

small airway disease leads to

A

airway inflammation and remodeling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

parenchymal destruction leads to

A

loss of alveolar attachments

decrease of elastic recoil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

thick, sticky mucus is more associated with

A

obstructive bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

air becoming trapped in damaged alveoli and air exchange becoming difficult is more associated with

A

emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

blue bloaters have

A

chronic bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pink puffers have

A

emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

chronic bronchitis presents more with

A
hypoxemia
respiratory acidosis
cor pulmonale from pulmonary hypertension
chronic bacterial colonization
airway hyper-reactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

chronic bronchitis is defined as

A

chronic productive cough for 3 or more months during 2 consecutive years with no other cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

structural changes that occur with chronic bronchitis

A

mucous gland enlargement causes hypersecretion
bronchial squamous metaplasia
loss of ciliary transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

inflammation in chronic bronchitis is mediated by

A

neutrophils

due to chronic bacterial colonization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

presents with inspiratory and expiratory obstruction

A

chronic bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

impeded ventilation in chronic bronchitis results in

A

hypoxemia

hypercapnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

has more parenchymal damage

A

emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

destruction of the alveolar walls in emphysema leads to

A

pathologic enlargement of the air spaces distal to the terminal bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2 possibilites for alveolar destruction in emphysema

A
  1. too much elastase

2. too little antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

protease enzyme secreted by neutrophils and macrophages during inflammation, destroys bacteria and host tissues

A

neutrophil elastase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

inhibits neutrophil elastase

A

alpha-1 antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

loss of alveolar supporting structure leads to

A

airway narrowing

compressed ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

presents with expiratory airflow obstruction

A

emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when is hypoxemia present in emphysema

A

later in disease

destruction of capillary bed leads to reduced DLCO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

asthma is mediated by

A

eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what cigarette smoking do

A

stimulates elastase

releases cytotoxic oxygen radicals from WBCs in lung tissye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

classic presentation of COPD

A

dyspnea
cough
sputum production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

most common symptom of COPD

A

dyspnea on exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

physical exam findings of COPD

A
tripod positioning
cyanosis
tobacco staining of fingers
JVD
accessory muscle use
pursed lip breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

for some reason Ms. Shamblen seemed to really care about this finding

A

tobacco staining of fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does pursed lip breathing help in emphysema

A

resistance to outflow raises intrabronchial pressure keeping the bronchi open longer to expel more air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

lung findings in COPD

A
barrel chest (increased AP diameter)
prolonged expiration
increased resonance
decreased breath sounds
wheezing
crackles at bases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

heart findings in COPD

A

S3 gallop

RV lift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

abdominal findings in COPD

A

hepatomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

extremities findings in COPD

A

muscle wasting

peripheral edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

cor pulmonale is

A

pulmonary hypertension resulting in impaired right ventricle dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what’s unique about cor pulmonale

A

it’s right ventricle dysfunction (hypertrophy, dilation) that ISN’T caused by left ventricle dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

required for diagnosis of COPD

A

spirometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

why are other labs done with COPD if spirometry is the diagnostic measure

A

to rule out other causes o dyspnea and comorbid diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

spirometry consistent with obstructive pattern

A

FEV1/FVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

other lung test findings with COPD

A

increased total lung capacity

38
Q

severe emphysema will have

A

decreased diffusing capacity of carbon monoxide

39
Q

why do you do a CBC

A

rule out anemia

40
Q

seen on CBC of chronic bronchitis

A

polycythemia

secondary to chronic hypoxia

41
Q

may be seen on CBC during acute exacerbations of CBC

A

leukocytosis

42
Q

when to assess pulse ox (SpO2) further when

and with what

A

SpO2 <92%

arterial blood gas (PaO2)

43
Q

PaO2 will probs show

A

mild/moderate hypoxemia without hypercapnia

severe disease: hypercapnia causing respiratory acidosis

44
Q

when to obtain a sputum culture

A

in patient unresponsive to initial antibiotic treatment

45
Q

what might be found on EKG

A

tachycardia
right atrial enlargement
right axis deviation and/or right ventricular hypertrophy

46
Q

CXR will show

A

signs of air trapping (increased AP diameter, hyperinflation, hyperlucency, flat diaphragms)
blebs or bullae

47
Q

CXR of chronic bronchitis

A

cardiac enlargement
pulmonary congestion
+/- perivascular or peribronchial markings

48
Q

pathognomonic for emphysema

A

blebs/bullae

49
Q

CXR findings suggestive of emphysema

A

hyperinflation +/- bullae
flattening of diaphragms
enlargement of retrosternal air space

50
Q

when to get a chest CT

A

symptoms suggest a complication of COPD (pneumonia, pneuomothorax, large bullae)
rule out alternate diagnosis (PE)

51
Q

when to get a high resolution CT

A

considering lung volume reduction surgery

52
Q

what’s the main goal of COPD management

A

prevent progression

53
Q

group A tx

A

short acting bronchodilator
-or-
SABA + SAMA combo

PRN

54
Q

group B tx

A

long acting bronchodilator (LAMA or LABA)

55
Q

group C tx

A

LAMA

56
Q

group D tx

A

LABA + LAMA
-or-
consider ICS + LABA

57
Q

albuterol is a

A

short acting beta agonist bronchodilator (SABA)

2 puffs q4-6 hours

58
Q

salmeterol is a

A

long acting beta agonist bronchodilators (LABA)

q12 hours

59
Q

side effect of B2 agonists

A
******
palpitations
tachycardia
insomnia
tremors
******
60
Q

side effects of anticholinergic bronchodilators

A

dry mouth
metallic taste
headache
cough

61
Q

ipratropium bromide

irpatropium + albuterol

A

short acting anticholinergic (SAMA)

2 puffs BID-QID

62
Q

the BA in SABA/LABA is

A

beta agonist

63
Q

the MA in SAMA/LAMA is

A

muscarinic antagonist (idk why they’re called anticholinergics in the lecture just to make it more confusing)

64
Q

tiotropium bromide

A

long acting anticholinergic (LAMA)

once daily

65
Q

what are anticholinergics good at

A

reduce air trapping

less cardiac stimulation

66
Q

whats the newest combo med for COPD tx

A

LAMA + LABA

67
Q

theophylline is

A

a methylxanthine

old drugs for COPD, not used much due to side effects, toxicity, drug-drug interactions

68
Q

when to use theophylline

A

refractory COPD

69
Q

Umeclidinium

A

long acting anticholinergic (LAMA)

once daily

70
Q

formoterol is a

A

long acting beta agonist bronchodilators (LABA)

q12 hours

71
Q

advair

A

inhaled corticosteroid

72
Q

dulera

A

inhaled corticosteroid

73
Q

symbicort

A

inhaled corticosteroid

74
Q

breo ellipta

A

inhaled corticosteroid

75
Q

corticosteroids MOA

A

inhibit prostaglandins –> reduced mucosal edema/inflammation –> decreased secretions

76
Q

corticosteroids side effects

A

oral candidiasis

bruising

77
Q

alpha 1 antitrypsin deficiency is defined as

A

serum levels <11 uM

78
Q

alpha 1 antitrypsin deficiency controversial tx

A

antiprotease replacement injections weekly/monthly

79
Q

gold stage B-D should also get

A

pulmonary rehab

80
Q

give O2 when
to reach the goal of
for how long

A

chronic dyspnea at rest
SpO2 > 90% all the time
12+ hours a day

81
Q

caution with O2 therapy

how to prevent it

A

high flow O2 may reduce drive to breath, causing respiratory acidosis
maintain O2 90-92%

82
Q

educate COPD pts to

A

recognize early signs of pulmonary infection

83
Q

early signs of pulmonary infection

A
increased sputum production
fever
worsening dyspnea
chest pain
hemoptysis
84
Q

what is
increased dyspnea
increased cough frequency/severity
increased or purulent sputum

A

acute exacerbation of COPD

85
Q

acute exacerbation of COPD is triggered by

A
respiratory illnesses (usually VIRAL)
pollution
86
Q

viral triggers of acute exacerbation of COPD

A

rhinovirus
influenza
may lead to secondary bacterial pneumonia

87
Q

most common bacterial pathogens in acute exacerbation of COPD/secondary bacterial pneumonia (unclear which she meant)

A
H influenzae
S pneumoniae
Moraxella cararrhalis
Mycoplasma pneumoniae
Pseudomonas aeruginosa
88
Q

starred bacterial pathogen

A

pseudomonas aeruginosa

89
Q

treatment of acute exacerbation of COPD

A
increase dose of SABA
can add ipratropium to regimen
Oral steroids (40 mg/day x 5 days)
90
Q

treatment of moderate/severe acute exacerbation of COPD

A

antibiotics:
Macrolide (azithromycin, clarithromycin)
Fluoroquinolone (moxifloxacin, gemifloxacin, levofloxacin)

91
Q

treatment of severe acute exacerbation of COPD

A

hospitalization

92
Q

indications to hospitalize

A
severe signs/symptoms
severe underlying COPD (FEV1 <50%)
significant comorbities
onset of new physical symptoms (cyanosis, edema, arrhythmias)
failure to respond to initial meds
older age
insufficient home support