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MS Pulm > Pulm > Flashcards

Pulm Flashcards

1
Q

4 types of CT

A
  1. Conventional CT
  2. High resolution CT
  3. Helical CT
  4. Electron Beam CT
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2
Q

Conventional CT for

A

Look at anatomy

Not really for lungs

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3
Q

High resolution CT for

A

Lung parenchyma at high resolution

ILD
Bronchiectasis

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4
Q

Does high resolution need contrast?

A

No

NOT to look at vessels

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5
Q

Use what CT to guide biopsies?

A

HRCT

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6
Q

Two types of helical CT

A

Single section CT

Multidetector CT

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7
Q

Does helical CT need contrast

A

Yes, IV contrast

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8
Q

Multidetector CT best way for

A

Performing CT pulmonary angio

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9
Q

Helical/MDCT 3 advantages

A
  1. Scan large section on single breath
  2. Collect image precisely when flow of contrast is in the system you are concerned about
  3. Narrowing of collimation thru chest so lung & hilar images are “High resolution”
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10
Q

Electron beam CT

A

Lower radiation than hCT
But more $$$$$
Initially for heart

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11
Q

Diagnose ILD or bronchiectasis with

A

HRCT

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12
Q

Work up solitary pulm nodule

A

hCT or HRCT

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13
Q

Diagnose PE

A

CTPA via hCT or MDCT

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14
Q

MRI

A

Tumor near blood vessel or nerves
Determining what is tumor and what is not
Rarely venous thrombosis

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15
Q

3 methods for lung biopsy

A
  1. Transbronchial
  2. Open lung
  3. VATS
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16
Q

Before lung biopsy use

A

Chest x-ray & HRCT

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17
Q

Lung biopsy to get diagnosis of

A 
Interstitial lung dz
Lymphangitic spread of CA
Eosinophilic pneumonia
Vasculitis
Certain infections
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18
Q

HRCT over lung biopsy usually enough for diagnosis for

A

ILD & IPF

Except in atypical cases

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19
Q

Gold standard for dx PE

A

Pulmonary angiogram

But rarely used because CT PA is very reliable

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20
Q

PET scan

A

Benign vs malignant pulm nodule

Infectious or inflammatory conditions

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21
Q

BAL normal findings

A

< 16% lymphocytes

No eosinophils

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22
Q

BAL: increased neutrophils

A 
IPF
Collagen Vasc Dz
Asbestosis
Suppurative infections
Granulomatosis with polyangitis
ARDS
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23
Q

BAL: Increased lymphocytes

A

Hypersensitivity pneumonitis

Sarcoidosis

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24
Q

BAL: increased eosinophils

A 
Acute & chronic eosinophilic PNA
ARDS
Churg Strauss
Loffler Syndrome
Tropical Eosinophilia
Parasites (ascariasis)
TB
Collagen Vasc dz
Malignancy
Drug reactions
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25
Q

BAL to diagnose PNA

A

PJP in AIDS
CMV pna–inclusion body
Disseminated TB or fungal infection
Dx PNA in ARDS

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26
Q

BAL: turbid PAS +

A

Alveolar proteinosis

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27
Q

BAL: Langerhans cells

A

Eosinophilic granulomatosis (histiocytosis x)

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28
Q

BAL: bloody with large amt of hemosiderin in alveolar macrophages

A

Diffuse Alveolar Hemorrhage

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29
Q

BAL: hyperplastic & atypical type 2 pneumocytes

A

Cytotoxic lung Injury

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30
Q

BAL: foamy changes with lamellar inclusion

A

Amiodarone induced disease

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31
Q

6 Causes of hypoxemia

A
  1. V/Q mismatch
  2. R-> L shunt
  3. Decreased alveolar ventilation
  4. Decreased diffusion
  5. High altitude
  6. Low mixed venous 02
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32
Q

V/Q mismatch as a cause of hypoxemia

Means?

A

Airspace inadequately perfused or perfused areas inadequately ventilated

Responds to oxygen!!!

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33
Q

Examples of V/Q mismatch

A

(Chronic lung diseases)

Asthma
COPD
Pneumonia, interstitial dz, pulm Vasc dz
Pulmonary HTN
PE
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34
Q

Right to left shunting as cause of hypoxemia.

Examples?

A

Hypoxemia due to perfusion of non ventilated alveoli.

ARDS
Intra-alveolar filling: PNA, pulm edema
Intracardiac shunt
Vascular shunt

Does NOT respond to oxygen

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35
Q

Decreased alveolar ventilation as a cause of hypoxemia

A

Seen with decreased TV or low RRs

High pCO2
Normal Aa Gradient

Drug overdose
Neuromuscular dz
CNS disorder

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36
Q

Decreased diffusion as accuse of hypoxemia

Examples

A

Low DLCO

ILD
Emphysema

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37
Q

Hypoxemia association with DLCO

A

DLCO < or = 30% of predicted

At Higher DLCO if rapid HR

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38
Q

Increased DLCO

A

Alveolar hemorrhage

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39
Q

What cause of hypoxemia improves with oxygen? Which does not?

A

V/Q mismatch: improves with 02

R–>L shunt: does not improved with 02

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40
Q

Aa gradient

A

Difference between the partial pressure of oxygen in alveoli and arterial blood

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41
Q

Normal Aa gradient

A

5-15

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42
Q

Aa gradient increases with

A

Age

Abnormal lung disease

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43
Q

Aa gradient in hypo ventilation and high altitude

A

Normal Aa gradient!

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44
Q

Aa gradient really only helpful when

A

Patient is breathing on room air

Because Aa gradient will increase as Fio2 increases

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45
Q

Formula for Aa gradient

A

Aa gradient:

149 - [PaO2 + (1.25 x PaCO2)]

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46
Q

Oxygen transport to tissues dependent on:

A

Cardiac output
Hemoglobin level
Hemoglobin saturation (Sa02)

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47
Q

PaO2 of 60mmhg results in Sa02 of?

A

> 90%

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48
Q

Oxygen saturation of hemoglobin is dependent on

A

Temperature
2,3 DPG
pH

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49
Q

High phosphorous affects 2,3 DPG

A

High phos –> High 2,3 DPG

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50
Q

What does it mean to “RIGHT” shift oxyhb dissociation curve?

A

RIGHT shift

Decreased hb affinity for oxygen

(So at same PaO2 you carry less O2)

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51
Q

What RIGHT shifts the curve?

A

TAP

Increased Temperature
increased Acidosis
Increased 2,3 dPg

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52
Q

CO does what to ODC

A

Left shifts curve

High affinity of CO for hemoglobin

Pulse ox does not distinguish between oxy and carboxyhb :(

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53
Q

What is methemoglobin?

A

Iron is oxidized from ferrous (fe2+) to ferric (fe3+)

So can’t hold onto o2 or co2 & curve LEFT shifted

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54
Q

What two things left shift ODC

A

CO

MetHB

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55
Q

Clinical effects of metHbemia

A

Perioral & peripheral cyanosis
Fatigue & dyspraxia
Coma & death

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56
Q

Treatment of metHbemia

A

100% 02 & methylene blue

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57
Q

Treatment of chronic hereditary metHbemia

A

1-2 grams daily vit c

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58
Q

Normal oximetry is inaccurate with?

A

CO

MetHb

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59
Q

Decreased affinity for hb and oxygen (or right shifting curve) means

A

Release of oxygen to TISSUe

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60
Q

DLCO is decreased by

A

Anything that interrupts the gas-blood 02 exchange

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61
Q

DLCO decrease implies

A

Loss of effective capillary alveolus interface

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62
Q

Causes of low DLCO

A

Emphysema
Interstitial lung disease
Pulmonary vascular disease
Anemia

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63
Q

What is the first parameter to decrease in interstitial lung disease?

A

DLCO

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64
Q

Follow DLCO when prescribing

A

Dangerous meds like

Amiodarone or
Lung toxic chemo

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65
Q

how do you determine emphysema from chronic bronchitis & asthma?

A

DLCO

Low: emphysema
Normal: asthma & bronchitis

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66
Q

Normal DLCO in asthma & chronic bronchitis because?

A

Even though there is bronchi construction there is NO alveolar disease

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67
Q

Increased DLCO in

A

Problems that increase effective blood flow lung

CHF
Diffuse Alveolar Hemorrhage
Pulmonary infarct
Idiopathic pulm fibrosis

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68
Q

Things you can check on spirometry (in office)

A

Lung volume capacity
Exp flow
Flow vol loops
Bronchodilator response

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69
Q

Need pulm function in lab for additional

A

TLC
DLCO
Methacholine challenge

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70
Q

What is an abnormal lung volume?

A

> 120%

<80%

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71
Q

TLC assesses

A

Interstitial lung disease

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72
Q

Exploratory flow rate assess

FEV1/FVC

A

Obstructive lung disease

<70%

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73
Q

Four basic functional volumes of which lung is made

A

RV: residual volume
ERV: expiratory reserve volume
TV: tidal volume
IRV: inspiratory reserve volume

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74
Q

RV is

A

Unused space

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75
Q

ERV is

A

Expiratory Reserve Volume

From full non forced end-expiration to full forced end-expiration

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76
Q

TV is

A

Tidal Volume

Used in normal unforced ventilation

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77
Q

IRV is

A

Inspiratory reserve volume

From normal unforced end-inspiration to full-forced end inspiration

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78
Q

What is a capacity?

A

2 more more of the basic volumes and more functional significance

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79
Q

Vital capacity is

A

The volume you have available for breathing

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80
Q

Formula for VC

A

VC= IRV + TV + ERV

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81
Q

TLC formula

A

TLC = VC + RV

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82
Q

COPD lung volumes

A

TLC normal or increased
VC decreased
Increased RV (barrel chest)

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83
Q

Restrictive disease

A

TLC decreased
Decreased VC
Decreased RV

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84
Q

FEV1/FVC ratios
Normal
Obstructive
Restrictive

A

FEV1/FVC

Normal: 0.8
Restrictive > 0.8
Obstructive: <0.8

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85
Q

Asthma can have what sort of FEV1/FVC

A

Normal
Or
Less 0.8 if acute attack

And it is reversible!!

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86
Q

Flow diagram for obstructive disease

A

Decreased expiratory flow
(Bc of increased airway resistance)

Scooping

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87
Q

Causes of obstructive lung disease

A

Asthma
Bronchiectasis
COPD
Cystic fibrosis

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88
Q

Flow diagram for restrictive lung disease

A

Similar to normal curve but offset right and smaller

No scooping

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89
Q

Restrictive dz and RV

A

Intrathoracic dz: ILD, parenchymal LOW RV

Extrathoracic dz: obese, kyphosis
NORMAL RV

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90
Q

2 reasons to do bronchodilator response

A

Determine of obstruction is responsive to beta agonist

Test current regimen efficacy

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91
Q

If testing PFT with bronchodilator for responsiveness

A

Withhold beta 2 agonist for 8 hours & theophylline for 12-24 hours before testing

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92
Q

Work up if chronic cough can include

A

Methacholine or bronchoprovocation challenge

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93
Q

First step in evaluation possible asthmatic

A

PFTs

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94
Q

If normal PFT in suspected asthmatic next step is

A

Bronchoprovocation

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95
Q

Asthmatics vs non asthmatics in bronchoprovocation test

A

Asthmatics bronchoconstrict at a VERY low dose if the irritant while non asthmatics do not

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96
Q

Are PFTs indicated in routine pre op exam?

A

NO

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97
Q

PFT & ABG indicated preop when:

A
  1. If surgery close to diaphragm (gb)
  2. If pt has mod or worse lung dz
  3. For lung ca or lung resection presurg eval
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98
Q

What indicates higher risk postoperative pulm complications in a patient with moderate or worse lung dz?

A

FEV1 <1L

Elevated pCO2

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99
Q

High risk of post op pulm complications for pt with lung cancer or lung resection pre surgical if PFTs?

A

FEV1 < 0.8L after surgery

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100
Q

Emphysema exp flow volume

A

Decreased expiratory flow volume

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101
Q

Emphysema expiratory flow volume tracing

A

Concave

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102
Q

Emphysema response to beta 2 agonist

A

<200mL improvement in FEV1 or FVC

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103
Q

Emphysema TLC and VC

A

Emphysema
Increased TLC
Reduced VC (hyperinflation with trapped air)

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104
Q

Emphysema DLCO

A

Decreased DLCO

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105
Q

Chronic bronchitis Exp flow volume

A

Chronic bronchitis decreased expiratory flow volume

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106
Q

Chronic bronchitis response to beta 2 agonist

A

Minimal response to beta 2 agonist

<200 mL improvement in FEV1 or FVC

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107
Q

Chronic bronchitis TLC & VC

A

Chronic bronchitis TLC slight increase

Normal or slight increase VC

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108
Q

Chronic bronchitis DLCO

A

Chronic bronchitis DLCO normal to slightly decreased

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109
Q

Asthma PFT

A

Normal if no active disease

Or decreased exp flow

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110
Q

Asthma exp flow vol loop tracing

A

Asthma exp flow vol loop tracing

Concave

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111
Q

Asthma response to beta 2 agonist

A

Asthma response to beta 2 agonist

Significant

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112
Q

Asthma TLC and VC

A

Asthma TLC normal or increased

VC normal or reduced

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113
Q

Asthma DLCO

A

Asthma DLCO normal

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114
Q

Interstitial lung dz FEV1/FVC

A

Normal to increased FEV1/FVC

115
Q

Interstitial lung dz exp flow vol loop

A

Interstitial lung dz exp flow vol loop

Straight or slightly convex

116
Q

Interstitial lung dz lung volumes

A

Interstitial lung dz volumes proportional all decreased

117
Q

Interstitial lung dz DLCO

A

Interstitial lung dz DLCO reduced

118
Q

Asthma triad

A

“Samter’s triad”

ASA sensitivity
Asthma
Nasal polyposis

119
Q

Treat allergic rhinitis with

A

Intranasal glucocorticoids

120
Q

Asthma is exacerbated by what comorbid conditions

A

Allergic bronchopulmonary aspergillosis
OSA
Stress

121
Q

What is the strongest identifiable predisposing factor for IgE mediated asthma?

A

Atopy

122
Q

Severity of airflow obstruction in asthma is classified how?

A

Intermittent or persistent

Persistent: mild, moderate, or severe

123
Q

Initial work up tests for asthma

A

FEV in 6 seconds
FVC
FEV1/FVC before and after bronchodilator

124
Q

What is a response to a bronchodilator?

A

Increase in FEV1 of > or = 12%
and
an increase of at least 200mL

125
Q

Do bronchoprovocation test in patient with normal spirometry if they also have one of following:

A

Chronic cough
Intermittent symptoms of cough/wheeze
Exertion all dyspnea of unknown cause

126
Q

3 types of challenge used to confirm diagnosis of asthma?

A

Methacholine challenge
Histamine challenge
Thermal (cold air) challenge

127
Q

Diagnosis if asthma in respect to challenge

A

Patient must both tighten up with the challenge and loosen up with subsequent bronchodilators

128
Q

How do you diagnose exercise induced bronchospasm?

A

Decrease in FEV1 of >/= 10% after graded exercise on treadmill or stationary bike

129
Q

The most effective treatment for most asthma

A

Stop exposure to any environmental agents that act as triggers

Or can take extra bronchodilator inhalation a before exposure

130
Q

Guidelines for management for what in patients with difficult to control asthma

A

Empirically manage GERD and allergic rhinitis

131
Q

GERD management in co-existent asthma

A

About intake of foods that lessen LES tone (etoh, caffeine, nicotine, peppermint)
No eating within 3 hours of bed
Elevate head if bed
PPIs

132
Q

Treat rhinitis with

A

Intranasal steroids

133
Q

Monitor peak expiratory flow (PEF) in what sort of asthmatics?

A

Moderate-severe asthma
Or
Patients who can’t reliably describe symptoms of exacerbation

134
Q

Symptom based monitoring is as effective as PEF in all asthmatics except

A

moderate to severe asthmatics or poor historian

135
Q

Quick relief meds for AE asthma (mild or intermittent)

A

SABA
Systemic corticosteroids
Anticholinergics

136
Q

Long term control meds for asthma

A 
ICS-most potent & most effective 
LABA
Mast cell stabilizers 
Leukotriene modifiers
Methylxanthines
Immunomodulators
137
Q

1st choice for rescue treatment of AE asthma

A

Inhaled SABA- albuterol

EVEN if patient routinely uses them at home

138
Q

What indicates poor control of asthma?

A

SABA use >2 days/week

139
Q

When are OCS indicated for AE asthma?

A

Peak flow <80% after 3 treatments of rescue SABA

140
Q

What drug has been shown to decrease the frequency if return visits to ER for asthma?

A

Oral CS

141
Q

When do you use oral vs IV steroids?

A

Oral = IV = IM bioavailability

Only use IV: respiratory failure or vomiting

142
Q

Types of anticholinergics for asthma treatment

A

Ipratropium- asthma

Tiotropium- copd

143
Q

Short vs long acting anticholinergics

A

Short acting: ipratropriun (for asthma)

Long acting: tiotroprium (for copd)

144
Q

How do anticholinergics work?

A

Decrease cGMP that relaxes contractions of bronchial smooth muscle

145
Q

Use ipratroprium for

A

Moderate to severe exacerbation of acute asthma

With SABA!!

146
Q

Anticholinergics are not used for treatment of

A

Chronic treatment if asthma

147
Q

Goal for Oxygen for AE Asthma?

A

Pa02 of at least 60mmhg
or
02 sat >/= 90%

148
Q

Preferred drug for treatment of persist asthma when not controlled with SABA?

A

ICS

BID = QID

149
Q

Benefit of spacer use for steroids

A

Decreases amount of drug deposited in oropharynx

Increased amount of drug reaching the lungs

150
Q

Preferred inhaled steroid during pregnancy

A

Budesonide

151
Q

SE of ICS

A

Easy bruising

Higher dose: oral thrush & dysphonia & recurrent pulmonary infxn

152
Q

Examples of LABA

A

Salmeterol

Formeterol

153
Q

How do LABA work?

A

Increase cAMP causing relaxation if bronchial smooth muscles

154
Q

Only use LABA after

A

ICS

155
Q

LABA is indicated for treatment of

A

Moderate to severe persistent asthma

(After treatment with ICS & SABA)

(Not for acute or mild asthma)

156
Q

Never use what asthma med as monotherapy?

A

LABA

Otherwise increases exacerbation & mortality

157
Q

Treatment options for exercise induced bronchospasm

A

LABA (not for daily use)

Albuterol
Cromolyn

158
Q

Examples of mast cell stabilizers

A

Cromolyn sodium

Nedocromil

159
Q

How to mast cell stabilizers work

A

Inhibit degradation of mast cells

Mild antiinflamatory effects from decreasing release of inflammatory mediators

160
Q

Drugs for daily control of exercise induced bronchoconstriction

A

Inhaled albuterol

Inhaled cromolyn

161
Q

What do leukotrienes do?

A 
Contract smooth muscles
Promote mucus production
Cause airway edema
Vasoconstrict
Stimulate arachidonic acid rease
162
Q

What releases leukotrienes?

A

Mast cell
Basophils
Eosinophils

163
Q

Examples of leukotrienes modifiers

A

Montelukast
Zafirlukast
Zileutin

164
Q

How does montelukast & zafirlukast work?

A

Leukotriene receptor antagonist

165
Q

How does zileuton work?

A

5-lipooxygenase pathway inhibitor

166
Q

Leukotriene modifiers may have side effect of

A

Eosinophilic vasculitis (churg strauss)

Never preferred treatment for adults more often used for kids

Less potent than ICS & less effective than LABA

167
Q

Example & mechanism of methylxanthine

A

Theophylline

Bronchodilator
Mild antiinflamatory by inhibiting PDE

168
Q

When do you use theophylline?

A

Adjunct to ICS for difficult to control asthmatics
For chronic use

NOT FOR ACUTE treatment
Inferior overall

169
Q

Therapeutic range if theophylline

A

5-15

170
Q

Signs if theophylline toxicity

A

N & V
HA
Tremulousness
Palpitations

Seizure
Hypotension
Cardiac arrhythmia

171
Q

What drugs increase theophylline levels?

A 
Cipro
Clarithromycin
Zileuton 
Allopurinol 
Mtx
Estrogen
Propranolol
Verapamil
172
Q

What drugs decrease theophylline levels?

A

AEDs
Rifampin
SJ wort
Smoking

(Can cause AE asthma)

173
Q

What drugs when given with theophylline can decrease the level of coadminstered drug?

A

Phenytoin

Lithium

174
Q

What immunomodulators are available for asthma

A

Omalizumab

Anti IgE mab blocking the receptors on mast cells and basophils

175
Q

When is omalizumab indicated?

A

Allergies & severe uncontrolled persistent asthma on high doses of an ICS & LABA

176
Q

Classification of asthma types based on FEV1/PEF

A

> /= 80%: intermittent or mild persistent

60-80%: moderate persistent

<60%: severe persistent

177
Q

Night time awakenings to classify asthma

A

1nt a week but not daily: moderate

Often 7nt/wk: severe persistent

178
Q

Diagnose COPD when

A

Large airway symptoms: dyspnea, cough, sputum

Irreversible airway obstruction

FEV1/FVC <0.70

179
Q

Smoking damages

A

Big airways
Little airways
Alveoli

180
Q

Large airway damage from smoking

A

“Bronchitis”

Cough & mucus production

181
Q

Small airway damage from smoking

A

Airflow obstruction with hyperinflation

182
Q

Smokers bronchioles are affected how?

A

Centriacinar

Upper lungs

183
Q

Alpha antitrypsin deficiency and effects on lungs?

A

Panacinar

Lower lungs

184
Q

Spirometry and COPD

A

FEV1/FVC: <0.70
Elevated RV
Elevated TLC
Decreased VC

Emphysema: low DLCO

185
Q

Definition of chronic bronchitis

A

Cough with sputum production for at least 3 consecutive months for at least 2 consecutive years

186
Q

If you see clubbing

A

Look for other lung pathology

I.e. IPF or lung cancer

187
Q

GOLD classification for COPD based on

A

FEV1

188
Q

GOLD classification into:

A

Mild: FEV1> or = 80%
Moderate: FEV1 50-80%
Severe: FEV1 30-49%
Very Severe: FEV1 <30%

189
Q

Update on GOLD criteria 2011 also now includes

A
  1. GOLD spirometry
  2. Severity of symptoms
  3. Risk of exacerbations
  4. Comorbidities
190
Q

A-D COPD classification

A

A: fewer symptoms, low risk exacerbations
B: more symptoms, low risk
C: fewer symptoms, high risk
D: more symptoms, high risk

191
Q

BODE index for COPD

A

B: BMI
O: airway Obstruction
D: Dyspnea
E: Exercise capacity

E = 6 min walk test

Higher BODE = increasing risk of death

192
Q

COPD pathology results in

A

Airway obstruction
Hyperinflation
Problems with gas exchange

193
Q

Best prognostic indicator in COPD

A

FEV1

194
Q

Best predictor of FEV1

A

Pack years of smoking

Normal age related decrease in FEV1 is 15-30mL/yr

COPD: 60-120mL/yr of lung function

195
Q

Smoking cessation & lungs best when?

A

Younger age before any loss of pulm function

196
Q

PaO2 in COPD falls when?

A

Late in disease

When FEV1 <50%

197
Q

Chronic retention of CO in COPD doesn’t occur until when?

A

Very late in disease

FEV1< 25%

198
Q

Cor pulmonale occurs only when in COPD?

A

After prolonged, marked reduction in FEV1 < 25% with severe, chronic hypoxemia

199
Q

Hypoxemia in COPD is due to?

A

V/Q mismatch

Responsive to O2

200
Q

Treatment for COPD

A

stop smoking!

SABA –> LABA –> ICS –> roflumilast

201
Q

In COPD never use what alone?

A

Do not use ICS alone

Always ICS and LABA

202
Q

Combo LABA & ICS has increased risk of

A

PNA

203
Q

When so you use roflumilast & how does it work?

A

GOLD 3 & 4

PDE 4 inhibitor

204
Q

When do you use theophylline in COPD?

A

COPD patients on max therapy

Adds slight bronchodilator effect to salmeterol

205
Q

What vaccines do COPD patients need?

A

Pneumococcal

Influenza

206
Q

When is Oxygen appropriate for COPD?

A

Resting PaO2 55%

207
Q

Oxygen therapy in COPD endpoint level is?

A

90%

208
Q

When using O2 in COPD how long?

A

Continuous x 24hr
Minimal at least 15hr/day

Re-eval patients places on oxygen 2 months after they are on a stable regimen of drug therapy

209
Q

Pulmonary rehab benefits in COPD

A

Improves symptoms
Improves quality of life
Reduces hospitalizations & days in hospital
Survival is improved

210
Q

When do patients need lung volume reduction surgery (LVR)?

A

Emphysematous patients with upper lobe disease & low exercise capacity

211
Q

What interventions affect COPD outcomes long term?

A

Oxygen
Smoking cessation
LVR surgery
Lung transplant

212
Q

In COPD bronchodilator refers to

A

Anticholinergics
Or
Beta agonist

213
Q

Treatment for group A COPD

A

Short acting bronchodilator

214
Q

Treatment for group B COPD

A

Long acting bronchodilator

215
Q

Treatment for group C COPD

A

ICS & long acting bronchodilator

If cant afford:
SA bronchodilator & theophylline

Also: roflumilast

216
Q

Treatment for group D COPD

A

ICS & long acting bronchodilator

Roflumilast

217
Q

How do you assess for AE COPD

A

CXR
EKG: PE
ABG

Don’t use spirometry or peak flows

218
Q

Signs of PE on EkG

A

S1Q3T3
New RBBB
RAD

219
Q

Treatment of AE COPD

A

SABA & anticholinergics
Systemic corticosteroids

If mod/severe ill with purulent sputum antibiotics

NPPV

220
Q

Organisms associated with AE COPD

A

Moraxella
Pneumococcus
H. Influenza
Pseudomonas: in GOLD 3&4

221
Q

When do you think about alpha antitrypsin deficiency

A

Rare
Young smokers with bullous COPD at lung bases
FH of liver & lung disease

222
Q

Gene for AAT

A

Pi locus
PiZZ - low low levels of AAT
Variable dz
Smoking worsens lung dz!

223
Q

How do you diagnose AAT?

A

Serum level of AAT

Genetic testing of Pi locus

224
Q

Treatment of AAT

A 
Weekly IV AAT
Stop smoking
Treat as COPD
Liver & lung transplant if needed
Vaccinations
225
Q

Selection criteria for AAT treatment

A

PiZZ
AAT < 11
Abnormal CT or spirometry
Non smoker or ex smoker

226
Q

What is bronchiectasis?

A

Persistent pathologic dilatation of bronchi caused by infection mediated inflammation and destruction of airway walls

Bronchi fill with mucus & pus and then become fibrotic

227
Q

Specific causes of bronchiectasis

A 
Infection 
Focal lung obstruction
Systemic diseases reducing mucociliary clearance or preventing adequate immune response
Inhaling toxin
ABPA
AAT deficiency
228
Q

Specific infections causing bronchiectasis

A 
Virus: adeno or influenza
Poorly treated staph or gram neg PNA 
Bordetella pertussis
TB
MAC
229
Q

What sort if focal lung obstructions cause bronchiectasis?

A

Endobronchial tumor a
Lymph nodes
Foreign bodies

230
Q

Systemic disease causing bronchiectasis

A

Decrease mucociliary clearance or prevent adequate immune response
(Thus allow colonization of bacteria)

CF
Ciliary dyskinesia
HIV/AIDS
Immunoglobulin deficiency

231
Q

How do you diagnose bronchiectasis?

A

HRCT

232
Q

How do you treat bronchiectasis?

A

10-14 days antibiotics
Driven by sputum data
Chronic prophylaxis only causes resistance
Surgical resection if massive hemoptysis or in resolving infxn

233
Q

Empiric abx for CF bronchiectasis

A

Oral ciprofloxacin or aminoglycoside

Plus parenteral antipseudomonal pcn

234
Q

What gene mutation causes CF?

A

CFTR gene on chromosome 7

CF transmembrane conductance regulator protein

235
Q

CFTR gene mutation causes what problems

A

Decrease Na absorption
Decreased Cl secretion

Lung mucus dehydrated & sticky & low in o2 ~> bacterial superinfxn

236
Q

Consider CF with what symptoms

A

Recurrent sinusitis
Nasal polyps
Weight loss
Chronic prod cough- thick purulent sputum
Recurrent exacerbations of febrile respiratory infxns requiring abx
Infertile

Clubbing & cor pulmonale

237
Q

Organisms in CF

A 
GNR
Staph
H. Influenza
Pseudomonas
Enteric GNR; proteus, E. coli & klebsiella
Wierd: burkholderia
Aspergillus
Non TB mycobacteria
238
Q

Spirometry for CF

A

Reduction in FVC & FVC1

Reversible until late disease

239
Q

How do you screen for CF

A

Elevated chloride in sweat

240
Q

Confirmatory test for CF

A

Nasal potential difference test

Genetic analysis

241
Q

How do you manage CF

A 
Aggressive pulm toilet
Pancreatic enzymes
Vitamins A, D, E, K
Culture guided antibiotics for exacerbations
Recombinant DNAase
Inhaled hypertonic saline
242
Q

How does DNAase work for CF?

A

Degrades accumulated DNA in airways & better airflow

243
Q

How does hypertonic saline work for CF?

A

Improve airway clearance

244
Q

What abx are commonly used for CF prophylaxis?

A

Inhaled aminoglycosides
Aztreonam
Oral azithromycin

245
Q

Complications of CF

A 
Respiratory failure
Pulm HTN
Cor Pulmonale
PTX
Hemoptysis
246
Q

Antibiotics for AE COPD

A

Amox/clavulanate
Azithromycin
Respiratory quinolones

Pseudomonas coverage for GOLD 3&4

247
Q

Clinical presentation of ILD

A 
Dyspnea
Diffuse dz on CXR
Restrictive PFT
Decreased DLCO
Elevated Aa gradient
248
Q

3 types of ILD

A

Occupational & environmental
Idiopathic interstitial pneumonia
Others

249
Q

3 groups of occupational/ environmental ILD

A

1) occupational & environmental
2) organic dust induced (byssinosis)
3) inorganic dust induced

250
Q

Hypersensitivity pneumonitis mechanism

A

Immune-mediated granulomatous reaction to organic antigens

Poorly formed granulomas are typical

251
Q

Types of hypersensitivity pneumonitis

A 
Moldy hay = "farmers lungs"
Pet birds = "bird fancier or breeder"
Grain dust - workers ingrain elevator
Isocyanates
Air conditioning systems
Crack cocaine
252
Q

Hypersensitivity pneumonitis presentation of symptoms

A

Acute
Subacute
Chronic forms

Insidious onset
Recurrent or persistent pneumonia
Exposure

253
Q

How do you diagnose hypersensitivity pneumonitis

A

By history!!

CXR: fleeting (infiltrates)

254
Q

Differential diagnosis for hypersensitivity pneumonitis

A

Eosinophilic pneumonia
Cryptigenic organizing pneumonia (COP)
Sarcoidosis

255
Q

How do you differentiate sarcoidosis & hypersensitivity pneumonitis?

A

BAL: both increased lymphocytes

Hypersensitivity pneumonitis: helper/suppressor ratio 4:1

256
Q

Treatment for hypersensitivity pneumonitis

A

Remove offending agents

Corticosteroids in acute dz

257
Q

Cause of organic dust ILD

A

Byssinosis

258
Q

Exposure to what cases byssinosis?

A

Cotton
Flax
Hemp dust

259
Q

Symptoms of byssinosis

A

Monday chest tightness

Early stage: occ chest tightness
Late stage: regular chest tightness toward end of 1st day of workweek

(Monday blues)

260
Q

Types of inorganic dusts causing ILD

A

“C As Be S”

Coal worker pneumoconiosis
Asbetos
Berylliosis
Silicosis

261
Q

4 types of asbestos associated dz

A

Benign pleural plaques
BAPE: being asbestos pleural effusion
Malignant mesothelioma
Asbestosis

263
Q

Being pleural plaques of asbestos

A

Asbestos exposure
Bilateral mid thoracic pleural thickening plaques & calcifications

Spares costophrenic angle & apex
BENIGN
Not manifestation of asbestosis

264
Q

BAPE

A

MC manifestation of asbestos exposure in first 10 yrs

Eosinophils in pleural fluid
Effusion: serous or bloody

265
Q

Malignant mesothelioma

A

Merely exposure!

Tumor of mesothelial cell of pleura

Latency >40 years
Rapidly fatal
Not associated with smoking

266
Q

Asbestosis

A

The pulmonary disease

Parenchymal fibrosis & resultant impairment

At the BASES

Smoking is synergistic :(

267
Q

Asbestosis can lead to what?

A

Squamous & adeno Ca

268
Q

What cancers are associated with asbestos?

A

Malignant mesothelioma (just exposure)

Squamous
AdenoCA

269
Q

Toes of silicosis disease

A

Simple nodular
Complicated nodular
Silicoproteinosis

270
Q

Silica and macrophage relationship

A

Silica integrated by alveolar macrophages renders them ineffective

271
Q

Anytime you see +PPD in pt with silicosis

A

Treat like Latent TB

+PPD makes diagnosis of latent TB

272
Q

All patients with silicosis have increased risk for?

A

TB & malignancy

273
Q

What is simple nodular silicosis

A

Fibrocalcified small nodules

Upper lung
Hilar nodules “eggshell calcification”
Carcinogen!

274
Q

Things affecting upper lung

A

Silicosis
Coal workers pneumoconiosis
Berylliosis
TB

275
Q

If symptoms of silicosis rapidly worsen think

A

TB

276
Q

What is complicated nodular silicosis?

A

Big nodules >1cm

Progressive, massive fibrosis

277
Q

What is silicoproteinosis

A

Overwhelming exposure causes it within 5 years

Alveoli fill with eosinophilic material (like PAP)

278
Q

Treatment for silicosis

A

Acute: steroids
Severe: lung transplant

279
Q

Types of coal worker pneumoconiosis

A

Simple
Complicated Progressive
Caplan syndrome

280
Q

Simple CWP progression correlates with

A

Amount of coal dust deposited in lungs

281
Q

Complicated CWP

A

Progressive massive fibrosis nodules >2cm

No hilar involvement

Not based on amt of coal deposited

282
Q

CWP treatment

A

None

Smoking accelerated dysfunction

283
Q

Calplan syndrome

A

Seropositive RA & massive CWP

Heralded by peripheral lung nodules in addition to upper field nodules

284
Q

Exposure to what causes silicosis

A 
Mining
Glasswork
Ceramics
Sandblasting
Brickyards
Foundaries

Latency 20-30 years

MS Pulm (4 decks)

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