Clinical Eval of Pts with Lung Disease Flashcards

1
Q

Normal RR (Current)`

A

12-14

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2
Q

Kussmaul breathing

A

Rapid, large-volume breathing indicating intense stimulation of the respiratory center, seen in metabolic acidosis

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3
Q

Cheyne-Stokes respiration

A

a rhythmic waxing and waning of both rate and tidal volumes that includes regular periods of apnea. Seen in patients with end-stage LV failure, neurologic disease, in normal people sleeping at high altitude.

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4
Q

bronchial lung sounds over periphery suggest

A

consolidation

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5
Q

globally diminished breath sounds suggest

A

obstruction

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6
Q

What is the difference between fine and course crackles?

A

Fine crackles (<20ms) are gas bubbling through fluid and are heard in pneumonia, obstructive lung disease, and late pulm edema.

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7
Q

Digital clubbing suggests

A

Pulmonary: chronic infection, malignancy of lung/pleura, chronic interstitial fibrosis.
Does not occur in COPD or asthma.
Can also occur in cyanotic heart disease, infective endocarditits, cirrhosis, inflammatory bowel disease.

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8
Q

Hypertrophic pulmonary osteoarthropathy

A

a syndrome of digital clubbing, chronic proliferative periostitis of the long bones, and synovitis. Seen in same conditions as digital clubbing but is particularly common in bronchogenic carcinoma.

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9
Q

Cyanosis suggests

A

increased amount of deoxyhemoglobin in capillary blood. This can be due to hypoxemia, but not always. In polycythemia, cyanosis will occur even in very mild hypoxemia. In anemia, cyanosis will not occur, even in severe hypoxemia. Basically if you see cyanosis, get an arterial blood p02 or Hg sat.

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10
Q

Two ‘indirect’ measurements of pulmonary hypertension are

A

CVP (by JVP) and assessment of lower extremity edema.

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11
Q

Expected FEV1/FVC in obstructive disease

A

Expected to be low due to increased resistance (FEV1 is low, FVC is high).

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12
Q

List some obstructive diseases

A

COPD, Asthma, bronchiectasis, bronchiolitis, upper airway obstruction

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13
Q

Expected FEV1/FVC in restrictive disease

A

Normal to increased (largely due to reduced FVC).

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14
Q

How to diagnose restrictive disease:

A

Total lung capacity must be reduced. Reduced FVC is suggestive, but not diagnostic.

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15
Q

List some restrictive diseases

A

Pulmonary fibrosis, phrenic nerve injury (reduces diphragmatic contraction), diaphragm dysfunction, neuromuscular disease, pleural disease (eg pleural effusion, pleural restriction), lung resection.

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16
Q

When do you order diffusing capacity?

A

When you suspect diffuse infiltrative disease or emphysema

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17
Q

How is DL(CO) useful in evaluating an AIDS patient with cough?

A

It is highly sensitive (but not specific) for pneumocystis. A normal DL(co) is evidence against pneumocystis.

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18
Q

When is an arterial blood gas indicated?

A

When acid-base disturbance, hypoxemia, or hypercapnia (high CO2) is suspected

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19
Q

When is pulse Ox inaccurate?

A

Anemia, hemoglobinopathy, when pulsatile arterial flow is disrupted.

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20
Q

Bronchial provocation testing

A

Useful in diagnosing asthma in pts with normal spirometry. A nebulized bronchoconstrictor is given. If FEV1 falls by more than 20% at a dose of less than 16mg/mL, then the test is positive. Sensitivity is high (95%) specificity is 70%.

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21
Q

When is a rigid bronchoscopy indicated?

A

Massive bleeding, extraction of large obstructing objects, biopsy of tracheal or main stem bronchus tumors. Requires general anaesthesia (unlike flexible bronchoscopy).

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22
Q

Acute upper airway obstruction: causes

A

trauma, foreign body aspiration, laryngospasm, laryngeal edema, infections (epiglottitis), acute allergic laryngitis.

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23
Q

What is the strongest identifiable predisposing factor for the development of asthma?

A

Atopy (allergy)

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24
Q

Exercise-induced bronchoconstriction

A

Begins during or within 3 minutes of exercise ending, peaks within 10-15 minutes, and resolves within 60 minutes. A consequence of airway’s attempt to warm and humidify additional volumes.

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25
Q

Why are asthma symptoms worst at night?

A

Circadian variations in bronchomotor tone increase bronchial symptoms between 3 and 4 AM.

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26
Q

What is the most common lab abnormality in asthma?

A

respiratory alkalosis

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27
Q

First steps if you suspect asthma

A

Spirometry. Compare results before and after administration of bronchodilator. If FEV1 increases by 12% or more OR FVC increases by 15% or more after bronchodilator, this confirms asthma. A negative test does not rule it out though. If Spirometry and bronchodilator tests are negative, move on to bronchial provocation testing.

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28
Q

Peak expiratory flow

A

Useful in asthma management and can be measured with handheld device. Measure once in the morning before taking bronchodilator and once in the afternoon after taking bronchodilator. 20% or greater increase means therapy is adequate.

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29
Q

What else is on your DDx with asthma?

A

Upper airway disorders (eg vocal cord paralysis), COPD, systemic vasculitides, psych

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30
Q

Define “control” and “responsiveness” in asthma therapy

A

Control is the degree to which symptoms and activity limitations are minimized by therapy.
Responsiveness is the ease with which control is achieved with therapy.

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31
Q

Differentiate between impairment and risk in asthma treatment

A

Impairment is the frequency and intensity of symptoms as well as functional limitations.

Risk is the likelihood of of acute exacerbation or chronic decline in lung function.

These two are not always related.

32
Q

What are the preferred controller treatments for patients with asthma?

A

Inhaled corticosteroids. Systemic corticosteroids may be necessary in patients with severe symptoms or refractory, poorly controlled asthma.

33
Q

Mediation inhibitors

A

long-acting bronchodilators useful in patients with mild persistant or exercise-induced asthma.

34
Q

Long-lasting Beta-adrenergic agonists

A

used in combination with inhaled corticosteroids for long-term prevention of asthma symptoms, nocturnal symptoms, and prevention of exercise-induced bronchospasm. As monotherapy, they actually increase risk of fatal asthma attacks.

Oral preps can also be used.

35
Q

Anticholinergics

A

add-on for patients who are not adequately controlled with inhaled corticosteroids AND beta2 agonists

36
Q

Phosphodiesterase inhibitors (Theophylline)

A

Can be added in poorly controlled moderate and severe asthma. Require close monitoring of plasma levels.

37
Q

Leukotriene modifiers

A

an alternative to inhaled corticosteroids for patients with mild-persistant asthma (though generally less effective).

38
Q

Omalizumab

A

recombinant antibody that binds to IgE without activating mast cells. Reduces need for corticosteroids in patients with moderate-to-severe asthma.

39
Q

Which vaccine can cause asthma exacerbation?

A

live attenuated influenza administered intranasally.

40
Q

First line for acute asthma exacerbation? Dose for mild, moderate, severe exacerbation?

A

Inhaled beta-agonists (eg albuterol). 1-2 MDI puffs is adequate for mild-to-moderate exacerbation. Severe exacerbation will require 6-12 puffs every 30-60 minutes.
Note that frequent use diminishes asthma controlling effect.

41
Q

What is used in patients who cannot take beta agonists or are suffering from bronchospasm due to beta blocker?

A

Anticholinergics (ipratropium bromide- similar to atopine)

42
Q

When are systemic corticosteroids prescribed for asthma?

A

They are used for treatment of acute exacerbation where patients who do not respond completely to beta-2-agonist therapy. They speed the resolution of airway obstruction and reduce rate of relapse.

Prescribe for home administration in patients with moderate or severe asthma.

43
Q

When do you use antibiotics in asthma patients?

A

NOT empirically. Use when you suspect actue bacterial respiratory infection (slightly lower burden of evidence than a healthy person).

44
Q

Patient has a mild exacerbation, what do you do?

A

Treat with short-acting beta 2 agonist until it resolves. Initiate inhaled corticosteroids if they have not already been initiated. If they have, consider adding a 7-day course of prednisone.

45
Q

What do you do in a severe asthma exacerbation?

A

Oxygen! (asphyxia is most common cause of death), inhaled short acting beta-2-agonsit (min 3 MDI or neb units), systemic corticosteroids, IV magnesium sulfate.

In ER, repeat assessment of patients should be done after 1st dose of inhaled bronchodilator, and again after 3 doses (60-90 minutes after tx initiation)

46
Q

What predicts the need for hospitalization best in asthma exacerbation?

A

The response to the initial treatment (NOT severity at presentation)

47
Q

Chronic bronchitis

A

clinical designation defined by excessive secretion of bronchial mucus with daily productive cough for 3 months or more in last 2 years.

48
Q

Emphysema

A

pathologic diagnosis that denotes abnormal permanent enlargement of the air spaces distal to the terminal bronchiole, with destruction of their walls.

Most patients with COPD have both chronic bronchitis and emphysema.

49
Q

What are some common complications of COPD

A

Acute bronchitis, pneumonia, pulmonary thrombembolism, atrial dysrhythmias, and left ventricular failure. In late stages, pulmonary HT is common.

50
Q

Treatment fundamentals for ambulatory patients with COPD

A
  1. Smoking cessation
  2. Oxygen therapy (the only one that actually improves disease natural history)
  3. Inhaled bronchodilators (anticholinergic, beta-2-agonist, or long-lasting beta-2-agonist).
  4. Inhaled corticosteroid (not oral)
51
Q

When is theophylline used in COPD control?

A

For patients who do not achieve adequate symptom control with inhaled anticholergenics, beta-2-agonists, AND corticosteroids. Improves Hg sat during sleep. Remember, it has a narrow therapeutic window.

52
Q

When should a COPD patient be given antibiotics?

A

When a patient has a COPD exacerbation associated with increased sputum purulence accompanied by dyspnea or an increase in the quantity of sputum. Make sure you cover Pseudomonas if it is plausible (previous isolation, FEV1<50% of expected, recent hospitalization 2 or more days in last 3 months, more than 3 courses of antibiotics in last year, or use of systemic corticosteroids).

53
Q

How should patients hospitalized with acute COPD exacerbation be treated?

A
  1. Supplemental oxygen
  2. Inhaled ipratropium bromide plus beta-2-agonists
  3. Oral corticosteroids
  4. broad-spectrum antibiotics

Do not begin Theophylline, but continue if patient is already taking it.

54
Q

When to admit for COPD?

A

Severe symptoms or acute worsening that fails to respond to OP management

Acute or worsening hypoxemia, hypercapnia, peripheral edema, or change in mental status

Inadequate home care

Presence of high-risk comorbid conditions

55
Q

Symptoms of bronchiectasis

A

chronic, productive cough (sputum is copius) with dyspnea and wheezing.

56
Q

What is bronchectasis?

A

disorder of the large bronchi characterized by permanent, abnormal dilation and destruction of bronchial walls. Can be caused by recurrant inflammation or infection of airways. CF is responsible for half of cases.

57
Q

Best imaging modality for COPD?

A

CT. Plain film is ok, but CT is diagnostic for emphysema.

58
Q

Radiographic findings of bronchiectasis:

A

Dilated, thickened airways (tram tracks or ring-like markings) and scattered, irregular opacities.

59
Q

What are the typical etiologies of bronchiectasis?

A

CF. Otherwise it is usually Haemophilus. Pseudomonas causes a rapid course, S pneumo and S. aureus are also common.

60
Q

How is bronchiectasis treated?

A

Antibiotics, daily chest physiotherapy with postural drainage and chest percussion, and inhaled bronchodilators. Always make sure to rule out pseudomonas and non-TB mycobacteria.

After treatment, consider prolonged macrolide therapy (eg Azithromycin 500mg 3x/week for six months).

61
Q

Cystic fibrosis: diagnostic essentials

A
  1. Chronic or recurrent productive cough, dyspnea, and wheezing.
  2. Recurrant airway infections with H. influenzae, Pseudomonas, S. aureaus with bronchiectasis and scarring on chest radiograph.
  3. Airflow obstruction on spirometry
  4. Pancreatic insufficiency, recurrent pancreatitis, distal intestinal obstruction, chronic hepatitis, nutritional deficiencies, or male urogenital abnormalities
  5. Sweat chloride concentration> 60mEq/L on two occasions or known gene mutation. (though this last one is all you technically need, absence of these does not r/o CF).
    other alternative diagnostic studies (such as measurement of nasal membrane potential difference, semen analysis, or assessment of pancreatic function) should be pursued, especially if there is a high clinical suspicion of cystic fibrosis.
62
Q

Symptoms of CF

A

Young adults with history of chronic lung disease (bronchiectasis), pancreatitis, or infertility. Often have chronic rhinosinusitis sx, steatorrhea, diarrhea, abdominal pain.

63
Q

Signs of CF

A

Pt wil be malnourished with low BMI.

May also see pulm findings of obstruction (AP-post ratio increased, hyperresonance, apical crackles).

Pt wil be malnourished with low BMI.

May also see pulm findings of obstruction (AP-post ratio increased, hyperresonance, apical crackles).

64
Q

CF lab findings

A

Hypoxemia, chronic compensated respiratory acidosis. Mixed obstructive/restrictive pattern on pulmonary function tests

65
Q

CF pulmonary function test findings:

A

Reduced FVC, airflow rate, and TLC.

66
Q

CF on imaging

A

signs of bronchiectasis, hyperinflation. Pneumothorax is common.

67
Q

Treatment principles for CF

A

clearance and reduction of lower airway secretions, reversal of bronchoconstriction, treatment of respiratory tract infections and airway bacterial burden, pancreatic enzyme replacement, and nutritional and psychosocial support (including genetic and occupational counseling).

68
Q

When are antibiotics indicated in CF?

A

Short term: to treat active airway infections based on results of culture and susceptibility testing of sputum. S aureus (including methicillin-resistant strains) and a mucoid variant of P aeruginosa are commonly present. H influenzae, Stenotrophomonas maltophilia, and B cepacia (a highly drug-resistant organism) are occasionally isolated.

Long-term: If positive for Pseudomonas ONLY. These antibiotics include azithromycin 500 mg orally three times a week, which has immunomodulatory properties, and various inhaled antibiotics (eg, tobramycin, aztreonam, colistin, and levofloxacin) taken two to three times a day. The length of therapy depends on the persistent presence of P aeruginosa in the sputum

69
Q

When should inhaled bronchodilators be used in CF treatment?

A

When their use has shown an increase of at least 12% in FEV1.

70
Q

Ivacaftor

A

an oral drug, available for the 5% of cystic fibrosis patients with a G551D mutation

71
Q

What is the only definitive treatment for advanced CF?

A

Lung transplant. Double-lung or heart-lung transplantation is required. A few transplant centers offer living lobar lung transplantation to selected patients. The 3-year survival rate following transplantation for cystic fibrosis is about 55%.

72
Q

What is a normal arterial blood pH?

A

7.4 (+/-0.02)

73
Q

What is a normal arterial blood pCO2?

A

40 mmHg

74
Q

What is a normal arterial blood HCO3?

A

24mmol/L (+/- 2mmol)

75
Q

Describe the approach to interpreting labs in acid base disorders:

A
  1. Is pt acidemic or alkalemic?
  2. Is it due to low/high pCO2?
  3. Is the pH change what we would expect (pH decrease= 0.08*(PaCO2 - 40)/10
  4. Is diffusion impaired? Determine A-a gradient–>
    150 (or whatever you calculate PAO2 to be) - PaCO2/0.8 = expected PaO2 if exchange is perfect (should be less than 5% from that).