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Respiratory Medicine Final > In-Class lecture material - Slocum > Flashcards

In-Class lecture material - Slocum Flashcards

1
Q

ATS recommends that every pt with dyspnea be evaluated for what 3 domains?

A
  1. sensory - intensity and quaility
  2. affective - unpleasantness or distress
  3. impact or burden - what level of impairment
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2
Q

Causes of wide A-aDO2

A
  1. V/Q mismatch
  2. Qs/Qt
  3. Diffusion abnormalities
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3
Q

what are the stages of spirometry classification of COPD

A 
Gold 1 (mild)  = FEV1 gr than 80% 
Gold 2 (moderate) = FEv1 50% to <80% 
Gold 3 (severe) = FEV1, 30-<50%
Gold 4 (very severe) = FEV1 <30%
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4
Q

Medical Research Council Dyspnea Scale

A

Grade 0 = breathless w/strenuous exercise
Grade 1 = SOB when hurrying on level or walking up slight hill
Grade 2 = On level ground, walk slower than normal cuz of breathlessness or have to stop for breath
Grade 3 = Stop for breath after 100 yds on level ground
Grade 4 = Too breathless to leave home, get breathless when dressing

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5
Q

What are the reasons for Dyspnea in COPD?

A
  • Increased dead space - -Increased PaCO2
  • Altered V/Q relationships - hypoxemia
  • Airflow obstruction
  • reduced mechanical advantage of diagragm
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6
Q

How does the volume/flow loop change in COPD?

A

During expiration (top half) the loop is scooped off indicating air is not flowing out as much. as efficiently

Normally, tidal flow volume loops expand in both direction during exercise. In emphysema, the decreased expiratory time (because of increased respiratory rate during exercise) results in more air trapping and increases the FRC, shifting the tidal flow-volume loop curves to the left, a phenomenon called dynamic hyperinflation

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7
Q

what are some common causes of hypoxemia with normal A-a gradient?

A

Alveoli are working fine, but you’re not inhaling enough O2. can be due to:
- hypoventilation (narcotics, neuromuscular weakness, obesity)
- high attitude
Can be treated with O2

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8
Q

what are some causes of hypoxemia with high A-a gradient?

A

Either due to 1)Alveoli cant get O2 to blood or 2) Blood is not going to working alveoli. Can be due to:

  • Pneumonia
  • PE
  • Chronic bronchitis
  • Pulm edema
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9
Q

what are the two common mechanism of creating a high A-a gradient?

A
  1. Fibrosis (loss of alveoli for diffusion, increased A-a gradient V/Q mismatch, hypoxemia
  2. Shunt (blood not flowing past alveoli with O2: anatomic shunting or physiologic shunting)
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10
Q

What are some examples of extrathoracic airway obstruction?

A

Obstruction upstream of the lungs.

- laryngeal inducable laryngeal obstruction, or laryngeal tumors.

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11
Q

Explain the changes seen in a flow loop due to a extrathoracic airway obstruction.

A

Normal expiratory flow loop, but when they try to inhale, the flow loop truncates (can’t generate flow). The reason is: if you exhale you create an intrathoracic/intraluminal pressure below the obstruction that is greater than Atm, as the diaphragm descends.

In other words, Extrathoracic airway obstruction is an INSPIRATORY problem.

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12
Q

Explain how the flow loop changes due to an intrathoracic obstruction (e.g. tumor in large airway)

A

when you inspire you create negative pressure inside thorax, and atm becomes significantly greater, thus inspiration is normal, but when you try to exhale you have to generate increased pressure than atm and this will result in a collapse of airway and thus truncate the expiratory flow loop.

in sum: intrathoracic obstruction is an expiratory problem

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13
Q

In order to qualify as significant response to a bronchodilator, what two criteria must be met after administration of an bronchodilator?

A
  1. 12% increase in VC or FEV1

2. 200cc increase in either VC or FEV1

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14
Q

which Gold Stages of dyspnea are oral PDE4 inhibitors (Roflumilast) and Theophyline used for?

A

Gold 3 and 4. stages before that are managed with ICS, SABA, SAMA, LABA and LAMA, any combo of those

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15
Q

Pts with COPD are often prescribed abx for which organisms?

A

H.Flu or morexella.

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16
Q

For milder and younger COPD pts with FEV1>50% and age <65 what abx are commonly used?

A
  • Doxycycline
  • TMP-SMX
  • Cephalosproin
  • Advanced macrolides (azithro or clarithro)
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17
Q

For sicker and older COPD pts which abx are commonly used?

A
  • Amoxi-clav

- Fluoroquinolones

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18
Q

In COPD pts what are criteria that which indicates supplemental O2

A
  1. PaO2 <56 t(7.3 Kpa) OR SpO2 <89% measure twice over a 3 week period of time
  2. PaO2 >56 <60 t (7.3 kPa) any time with evidence of: Pulm HTN, CHF, Polycythemia Hct >55%
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19
Q

How is mild COPD treated?

A

Either SABA or SAMA prn often ordered together as Combivent (difference between COPD and asthma is ICS indications)

20
Q

How is moderate COPD treated?

A

LABA or LAMA

21
Q

How is severe COPD treated?

A

ICS+LABA or ICS +LAMA (never use ICS alone in COPD)

-can be w/wo Roflumilast or theophylline

22
Q

How is very severe COPD treated?

A

ICS+LABA or ICS+LAMA or ICS +LAMA +LABA

w/wo roflumilast or theophylline

23
Q

What is the 6 minute test?

A

Assesses distance walked over 6 minutes as a sub-maximal test of aerobic capacity/endurance.
-Pt on room air walks for 6 mins and measure how far they can walk. Then let them rest for about 20 mins. And then give them O2 via nasal canula and again do the 6MWT and see if they do better.

24
Q

Inhalers and other meds are used to treat symptoms which decreases hospitalization and increases quality of life. What two factors is known to increase longevity in a COPD pts?

A
  • STOP smoking

- Supplemental O2

25
Q

Of the following, which has the greatest improvement in symptoms control in COPD patient?

  1. SABA or SAMA
  2. LABA or LAMA
  3. ICS+ SABA
  4. 6MWT
  5. Pulmonary rehab
A
  1. Pulm rehab
26
Q

what are the 5 physiologic reason for hypoxemia?

A
  1. Altitude
  2. Diffusion
  3. V/Q mismatch
  4. Hyperventilation
  5. Shunt
27
Q

In a pt with advanced COPD, what Xray findings are you likely to see?

A
  • Flattened diaphragm
  • increased retrosternal space
  • hyper inflation
  • bullous formation
28
Q

Inducible laryngeal obstruction is associated with which conditions?

A
  • Asthma
  • GERD
  • Chronic rhinosinusitis
29
Q

ILO and asthma are often confused. what are some salient differences?

A

ILO is rapid, waxes and wans and can leave abruptly, monophonic inspiratory stridor and prolonged inspiratory phase; limited to upper airway.

Asthma: not rapid, generally prolonged and never leaves abruptly; polyphonic expiratory with increased expiratory phase; lower airways

ILO treated with speeth therapy and avoidance of irritants. Asthma with ICS, SABA, LABA etc

30
Q

What are the prototypic interstitial lung disease (ILD) presentation?

A
  • Dyspnea
  • cough
  • Crackles often described as velcro
  • Digital clubbing
  • Exercise induced hypoxemia
  • PFT- reduced FRC, TLC normal FEV1/FVC ratio, low DLCO
31
Q

ILD evaluation must include history of:

A
  • occupation
  • hobby
  • environmental
  • travel
  • drugs both Rx and nonRx
32
Q

How is ILD evaluated?

A
  • Chest CT
  • PFT
  • ANA and Rheumatoid factors
33
Q

How does scleroderma present as a lung manifestation?

A
  • Pulmonary fibrosis
  • Pulm HTN - concentric fibrosis of vessels
  • Aspiration - esophgeal disease
34
Q

How does Rheumatoid arthritis present in the lung?

A
  • Interstitial pulm fibrosis
  • Bronchiectasis
  • Pulm Rheumatoid nodules
  • Pulm vasculitits
  • Pleural disease
35
Q

How does SLE present in lung?

A
  • Interstitial lung disease
  • Extra-pulm restriction
  • pulm HTN
  • Pleural disease
36
Q

what two drugs commonly cause lung fibrosis?

A
  • Amiodarone (Antiarrythmic agen)

- Nitrofurantoin (abx for UTI)

37
Q

How does hypersensitive pneumonitis present inthe acute and in the chronic form?

A

Acute: abrupt onset of dyspnea, cough, fever, maylagis. CXR shows pulm infiltrates. responds well to prednisone.

Chronic: pulmonary fibrosis. poor response to prednisone

38
Q

How is ILD treated?

A
  • treat or remmove underlying cause
  • Corticosteroids
  • Idiopathic pulm fibrosis: Pirfenidone and Nintedanib
39
Q

Pts with ILD due to what presents with erythema nodosum seen in Lofgrens syndrome?

A

Sarcoidosis

40
Q

What are the components of virchow’s triad?

A
  • Hypercoagulable states
  • Venous stasis
  • Intimal wall injury
41
Q

A young male develops acute SOB. Exam is normal. Normal PFTs. CXR is normal. Suspected to have a PE, how should pt be evaluated?

A
  1. D-dimer
  2. V/Q lung scan
  3. Chest CTA
  4. Pulm angiogram
42
Q

When evaluating pulmonary hypertension what imaging modality is MOST helpful?

A

ECHO. look for increased estimated PA pressures; peak tricuspid regurg velocity (generally greater than 3L/s

43
Q

What is the classification of Pulmonary HTN?

A 
Group 1 = Idiopathic and CTD
Group 2 = Heart
Group 3 = Lung
Group 4 = PE
Group 5 = All others
44
Q

How is Bronchiectasis managed?

A
  • Tracheobronchial clearance techniques (mechanical valves; postural drainage and chest physiotherapy, therapeutic vest)
  • Mucus-mobilizing methods
  • anti-inflammatory airway management
  • Anti-aspiration methods
45
Q

Findings of what marks exudate vs a transudate

A
  • Pleural protein/serum protien >.5
  • Pleural LDH/serum LDH >.6
  • pleural fluid >2/3 upper limit of serum level in lab doing the measurement
46
Q

A lymphocytic (>50%) effusion in pleural space is commonly due to

A

malignancy or TB

47
Q

what are common cause of transudative pleural effusion?

A
  • LVH or CHF
  • Other: mislaced TPN line, massive cirrhosis, nephrosis

For everyting else think exudative pleural effusion

Respiratory Medicine Final (14 decks)

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