PULMO-COPD Flashcards

1
Q
MC smoking 80-90% cases, 10x likely
Heredity (α-1 anti-trypsin deficiency)
Second-hand smoke 
air pollution (work/environment)
childhood respiratory infections
A

Risk factors COPD

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2
Q

S/S COPD

A

Chronic cough and sputum production,
DOR and DOE
H/o inhalation exposure
Persistent, progressive and exacerbated U/LRI
Irreversible inflammatory damage- airways, alveoli

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3
Q

PE

A

Cor pulmonale – alteration of RV fx or structure d/t pulmonary HTN , RHF, JVD, PEdema, Hepatomegaly
Breath sounds diminished d/t hyperinflation
Heart sound distant
Inc. (AP) thoracic diameter and low diaphragms
Impairment of expiratory airflow – “air trapping”
Destruction of lung parenchyma
Inc. accessory muscles,

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4
Q

Pulmonary Function Tests
Measurement of lung volumes
Quantitation of diffusing capacity of CO (DLCO)
Pulse oximetry

A

DLCO – diffusing capacity of the lungs for carbon monoxide; measures ability of lungs to transfer gas. low DLCO d/t dec. gas exchange from destruction of alveoli –
Narrow ddx of lung disease
air gets trapped in the lungs but gas exchange is not happening in ideal
Lung volumes N, but with hyperinflation
Decreased peak flow rate
Pulsus paradoxus- abnormally large decrease in stroke volume, >10mmhg drop inspiration. HR- dec inhale, exhal inc. (severe COPD attacks)

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5
Q

Obstructive pattern
Required for DX and evaluation
Reduced FEV1
Dec FEV1/FVC ratio
FVC may be normal with mild- becomes reduced with progressive disease secondary to air trapping
Increased RV lung volume to total lung capacity; hyperinflation

A

Spirometry in COPD

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6
Q
Dec vasculature markings
Squeezed cardiac siloquette
Darker Lungs (air trap)
Flatten diaphragm
Bulle
Hyperinflation
A

What determinants are on a CXR for emphesema?

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7
Q

Emphysema

A

Compliance work is increased ,elastic recoil is dec.(alveoli destroyed elastic)
P-V curve is shifted up and left. causing air trapping

CW-Less in asthma (constricted) slight in chronic bronchitis.

enlargement of the distal air spaces

Hypercapnia-Loss of alveolar capillary surface area

s/s-dyspnea, hyperinflation, irreversible airflow abnormalities

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8
Q

Chronic Bronchitis

A

Chronic, productive cough >3mo mo over 2y consecutive

ETI-Smooth muscle hypertrophy, inflammation, and plugging small airways with mucus

Obstruction somewhat reversible with β-agonists

S/S-may significant hemoptysis
Must r/o neoplasm

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9
Q

Diagnosing COPD

A

Chronic cough- intermittently, throughout the day
Rare nocturnal
Chronic Sputum Production

Dyspnea-worsening over time,“increased effort to breath,” “heaviness,” “air hunger,” or “gasping”
Worsens with exercetion, URI/LRI

History of exposure to:
Tobacco smoke
Occupational dusts/chemicals
Smoke from heating or cooking fuels

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10
Q

Polycythemia in Pts with chronic hypoxia; ABG: respiratory acidosis w/ hypoxemia

FEV1 and FVC - detects degree of obstruction

Staging system- classification of severity of airflow limitation; guide to management; assessing for significant hypoxia

A

Labs

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11
Q

GOLD Staging for COPD Severity Stage 0

A
Stage 0
At risk
Normal spirometry
Chronic symptoms
Cough
Sputum production
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12
Q

GOLD Staging 3

A
Severe COPD
FEV1/FVC < 70% of predicted
FEV1 < 30% of predicted
Sx of right heart failure
severe hypoxemia
Increased mortality
Obtain consultation
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13
Q

GOLD Staging 4

A
Very severe COPD
FEV1/FVC < 70% of predicted
FEV1 < 30% of predicted or FEV1 < 50% of predicted and symptoms of chronic respiratory failure
PaO2 < 60mmHg 
(+/-) PaCO2 > 50mmHg
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14
Q

Bring it up every visit
Discuss strategies to quit
Ask if patient ready
What has worked, what hasn’t, identify obstacles
Counseling, family/network support
1-800-NO-BUTTS
Nicotine replacement products
Chantix- effective $$$$, but ADE- Mental dz
Wellbutrin for cravings- helpful long term

Stop early better
never too late to stop- can see lung improvement

A

Smoking Cessation Management

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15
Q

stable COPD
#1 Inhaled β-adrenergic (SNS) agonists, short and long term
Anticholinergic bronchodilators may be used in combo

A

Bronchodilators

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16
Q

Corticosteroids

A

may have adverse side effects and have not been shown to benefit most COPD

Proven beneficial up to 2 weeks in acute exacerbations of chronic bronchitis

17
Q

Antibiotics

A

acute exacerbation- inc. volume and purulence of sputum

1st- doxycycline, cefuroxime or amoxicillin-clavulanate; 2nd line azithromycin
Antibiotics accelerate improvement in peak ERV, lessen the rate of relapse

Repeat infections contribute to inflammatory airway narrowing and damage to surrounding alveoli by the release of proteases or free radicals from PMN’s

Superinfection is common with H influenza, S pneumoniae, M catarrhalis, Mycoplasma pneumoniae

18
Q

Acute hypoxemia=acute exacerbations of COP
Supplemental O2 acute therapy
Pulse oximetry <88% for continuous (qualify)
Goal-Target PaO2 of 60-65, O2 saturation > 90%
Prolongs life

A

Oxygen Therapy

19
Q

Rehab-Increase exercise capacity, improve QOL
Multi-disciplinary, “group therapy”,
Exercise studies show no change in VO2max but higher workload (better efficiency)

Nutrition-protein deficiencies, emphysema low, d/t inc. work

LVRS or lung transplant, lung volume reduction surgery (removal of portion of diseased lung)

Prevention- Pneumovax, Influenza vaccine

Patient education

A

Therapy

20
Q

Polycythemia –
Hct >52% in men, 48% in women;
Hgb >18.5 in men, 16.5 in women; most often due to hypoxia

ABG Normal values — normal pH is 7.36 to 7.44,
PCO2 is 36 to 44 mmHg,
HCO3 21 to 27 mEq/L

A

Labs Blood norms

21
Q

reduced the number of patients who require arterial blood gases (ABGs).

does not provide information about alveolar ventilation or hypercapnia (PaCO2 >45 mmHg),

inaccurate in the setting of an acute exacerbation of COPD.

A

Pulse oximetry

22
Q

The indications for measuring ABGs

A

arterial oxygen tension [PaO2],

carbon dioxide tension [PaCO2]

acidity [pH])

Low (FEV1) <50 percent predicted

Low pulse oximetry <92 percent

Depressed level of consciousness

23
Q

Assessment for hypercapnia in at risk patients 30 to 60 minutes after initiation of supplemental oxygen

disease progresses_hypoxemia becomes severe_ hypercapnia may develop.

Hypercapnia likely when the forced FEV1 falls below one liter.

ABG worsen during acute exacerbations and may also worsen during exercise and sleep.

A

Acute exacerbation of COPD

24
Q
LAMA (anticholinergic) – Spiriva
SAMA (anticholinergic) – Atrovent
LABA (beta-agonist) – Serevent, Flovent
Combo anticholinergic/beta-agonist – DuoNeb, Combivent
Combo LABA/ICS – Advair
A

NIH Drugs

25
Q

COPD umbrella term

A

ICD 10
Many other cause
4th Leading cause of death

All have ICD10
Emphsema
asthma
Chronic broncitis

26
Q

Pink Puffers- Emphesema

A
No bronciitic component
Barrel chest
Dyspena early
Hunched over
 Hyperventilatin
Adquate O2
Weigh loss-Acid Base, wasting energy to get air in, malnourished
Quiet breath sounds
Older
27
Q

Blue Bloater-Chronic Bronchitis

A
Bronchitis component cough mucus
No barrel chest
Dyspnea late
No air hunger
Ventilation ok- Inc HgB
Cyanosis -toes fingers
Cor pulmonate- RHF
Obese
Wet
Wheezing
28
Q

Stage 1

A
Mild COPD
FEV1/FVC < 70% of predicted
FEV1 ≥ 80% of predicted
Mild airflow limitation
Minimal symptoms
Not at increased risk for mortality
29
Q

Stage 2

A
Moderate COPD
FEV1/FVC < 70% of predicted
FEV1 < 50% of predicted
Moderate symptoms of chronic cough, sputum production
Mild hypoxia
Obtain pulmonary consultation
30
Q

BODE index for survival predictions

Dyspna scale

A

Higher the points= lower risk for survival