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PSBIM > PULMONOLOGY > Flashcards

PULMONOLOGY Flashcards

1
Q

Most common site of bleeding in hemoptysis

A

Bronchi or medium-sized airways

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2
Q

Unique feature of the lung that predisposes to hemoptysis of varied severity

A

Dual blood supply

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3
Q

Dual blood supply of the lung

A

Pulmonary circulation

Bronchial circulation

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4
Q

Most common cause of blood-tinged sputum and small-volume hemoptysis

A

Viral bronchitis

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5
Q

Leading cause of massive hemoptysis and subsequent death

A

Bronchiectasis

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6
Q

Most common cause of hemoptysis worldwide

A

Tuberculosis

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7
Q

Most frequent source of bleeding in the hemoptysis in tuberculosis

A

Cavitary disease

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8
Q

Rare cause of hemoptysis where there is erosion of a pulmonary artery aneurysm into the preexisting cavity

A

Rasmussen’s aneurysm

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9
Q

A disease that mimic tuberculosis and acquired from raw crayfish ingestion

A

Paragonomiasis

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10
Q

Cyclical hemoptysis

A

Catamenial hemoptysis

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11
Q

Cause of catamenial hemoptysis

A

Pulmonary endometriosis

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12
Q

First step in evaluating hemoptysis

A

Determine the amount or severity of bleeding

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13
Q

Definition of massive hemoptysis

A

Blood loss of 400 mL in 24 hours or 100-150 mL expectorated at one time

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14
Q

If the chest radiograph of patient with hemoptysis is normal and no risk factors for malignancy, how will you treat the patient?

A

Treat as bronchitis and ensure close follow-up

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15
Q

3 simultaneous goals if with massive hemoptysis:

A

Protect the non-bleeding lung
Locate the site of bleeding
Control the bleeding

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16
Q

How will you position a patient with massive hemoptysis?

A

Patient should be positioned with the bleeding side down to use gravitational advantage to keep blood out of the non-bleeding lung

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17
Q

Procedure of choice for control of massive hemoptysis

A

Bronchial artery embolization

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18
Q

Complication of bronchial artery embolization

A

embolization of the anterior spinal artery

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19
Q

Ideal candidate for surgical resection in patients with hemoptysis:

A

Localized disease but otherwise normal lung parenchyma

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20
Q

Endotracheal intubation must always be done in treatment of massive hemoptysis: True or false

A

Endotracheal intubation should be avoided unless truly necessary (Suctioning through the ET tube is a less effective means of removing blood and clot than the cough reflex)

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21
Q

If endotracheal intubation is necessary in hemoptysis, what are two techniques that will protect the non-bleeding lung?

A

Selective intubation of one lung (i.e. the non-bleeding lung)
Insertion of a double-lumen ET tube

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22
Q

Etiology of primary lung abscess

A

Anaerobic bacteria / aspiration

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23
Q

Duration of acute lung abscess and chronic lung abscess

A

<4-6 weeks

> 6 weeks

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24
Q

Major risk factor for primary lung abscesses

A

Aspiration

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25
Q

Lung abscesses also arise from septic emboli from what endocarditis?

A

Tricuspid valve endocarditis

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26
Q

An infection begins in the pharynx (classically involving Fusobacterium necrophorum) then spreads to the neck and the carotid sheath (which contains the jugular vein) to cause septic thrombophlebitis

A

Lemierre’s syndrome

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27
Q

Most common locations of primary lung abscess

A

Posterior upper lobes and superior lower lobes – dependent segments

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28
Q

Which lung is usually affected in lung abscess?

A

Right lung (Right mainstem bronchus is less angulated)

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29
Q

With foul-smelling breath, sputum, or empyema and essentially diagnostic of an anaerobic lung abscess

A

Putrid lung abscess

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30
Q

Most common organisms causing secondary lung abscess

A

Pseudomonas aeruginosa and other gram-negative rods

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31
Q

More fulminant course of lung abscess with high fever is usually caused by

A

S. aureus

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32
Q

DOC for primary lung abscess

A

Clindamycin 600 mg q8hrs and IV β-lactam/β-lactamase combination

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33
Q

Duration of treatment of primary lung abscess

A

3–4 weeks to as long as 14 weeks

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34
Q

Size of lung abscess that is less likely to respond to antibiotic therapy without additional interventions

A

> 6-8 cm

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35
Q

Poor prognostic factors for lung abscess (5)

A 
	Age of >60
	Presence of aerobic bacteria
	Sepsis at presentation
	Symptom duration of >8 weeks
	Abscess size of >6 cm
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36
Q

Where is the cough center located?

A

nucleus tractus solitarius

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37
Q

Maximal expiratory pressure at the mouth is called:

A

Peak expiratory flow

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38
Q

Surrogate marker for cough strength

A

Peak expiratory flow

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39
Q

Duration of acute cough

A

< 3 weeks

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40
Q

Duration of subacute cough

A

3-8 weeks

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41
Q

Duration of chronic cough

A

> 8 weeks

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42
Q

Kind of cough that lingers for >2 months following one or more respiratory tract infections

A

Post-bronchitic cough

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43
Q

How many % of patients taking ACE inhibitors has persistent cough?

A

5-30%

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44
Q

How long will you wait for a decrease in cough after you discontinued ACEi in order to say that it is an unlikely cause of the cough?

A

1 month

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45
Q

Most potent cough suppressants

A

Narcotic cough suppressants (codeine and hydrocodone)

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46
Q

2 sleep-related breathing disorders and what is more common

A
  1. Obstructive sleep apnea/hypopnea syndrome (OSAHS) – more common
  2. Central sleep apnea (CSA)
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47
Q

Definition of OSAHS

A
  1. Either symptoms of nocturnal breathing disturbances (snoring, snorting, gasping, or breathing pauses duråing sleep) or daytime sleepiness or fatigue that occurs despite sufficient opportunities to sleep and is unexplained by other medical problems
  2. Five or more episodes of obstructive apnea or hypopnea per hour of sleep documented during a sleep study
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48
Q

Apnea-hypopnea index (AHI) calculated as

A

the number of episodes divided by the number of hours of sleep

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49
Q

Apnea-hypopnea index that can be considered as OSAHS even if with no symptoms

A

> 15 episodes/h

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50
Q

OSAHS severity is based on (5)

A
  1. Frequency of breathing disturbances (AHI)
  2. Amount of oxyhemoglobin desaturation with respiratory events
  3. Duration of apneas and hypopneas
  4. Degree of sleep fragmentation
  5. Level of daytime sleepiness or functional impairment
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51
Q

Pharyngeal airway has no bone or cartilage, hence, airway patency is dependent on the stabilizing influence of the

A

pharyngeal dilator muscles

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52
Q

Most common site of airway collapse in OSAHS

A

Soft palate

Other sites:

  1. Tongue base
  2. Lateral pharyngeal walls
  3. Epiglottis
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53
Q

OSAHS may be most severe during what stage of sleep and what position?

A

REM (rapid eye movement) sleep - neuromuscular output to the skeletal muscles is particularly low

Supine position

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54
Q

REM (rapid eye movement) sleep - neuromuscular output to the skeletal muscles is particularly low

Supine position

A
  1. Ventilatory sensitivity
  2. Arousal threshold
  3. Neuromuscular responses to CO2
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55
Q

Major risk factors for OSAHS (2):

A
  1. Obesity
  2. Male sex

Absence of obesity does not exclude this diagnosis

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56
Q

10% weight gain is associated with a ____ increase in apnea-hypopnea index

A

> 30%

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57
Q

Reasons why male sex is a risk factor for OSAHS (2)

A
  1. Android patterns of obesity

2. Relatively greater pharyngeal length

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58
Q

Additional risk factors for OSAHS aside from male sex and obesity (6)

A
  1. Mandibular retrognathia and micrognathia
  2. Positive family history of OSAHS
  3. Genetic syndromes that reduce upper airway patency
  4. Adenotonsillar hypertrophy (especially in children)
  5. Menopause
  6. Various endocrine syndromes
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59
Q

The most common complaint of OSAHS

A

Snoring

however, its absence does not exclude the diagnosis

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60
Q

Symptoms reflecting termination of individual apneas with abrupt airway opening in OSAHS

A

Gasping

Snorting

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61
Q

Generally distinguishes OSAHS from paroxysmal nocturnal dyspnea, nocturnal asthma, and acid reflux with laryngospasm

A

Absence of dyspnea

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62
Q

The most common daytime symptom of OSAHS is

A

excessive sleepiness

many women preferentially report fatigue rather than sleepiness

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63
Q

The gold standard for diagnosis of OSAHS is

A 
overnight polysomnogram (PSG) 
A negative in-laboratory PSG usually rules out OSAHS
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64
Q

The key physiological information collected during a sleep study for OSAHS assessment includes (4)

A
  1. measurement of breathing (changes in airflow, respiratory excursion)
  2. oxygenation
  3. body position
  4. cardiac rhythm
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65
Q

Measure in sleep study that includes the number of respiratory effort-related arousals in addition to the number of apneas plus hypopneas

A

respiratory disturbance index

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66
Q

Arousal index in sleep study is measured by

A

frequency of cortical micro-arousals or awakenings per sleep hour

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67
Q

Overnight blood pressure monitoring in OSAHS often displays what pattern

A

“non-dipping” pattern

absence of the typical 10-mmHg fall of blood pressure during sleep compared to wakefulness

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68
Q

It is the most common medical cause of daytime sleepiness and negatively influences quality of life

A

OSAHS

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69
Q

the standard medical therapy with the highest level of evidence for efficacy for OSAHS

A

CPAP

Other management:
Oral appliances – for mild OSAHS
Upper airway surgery
Bariatric surgery

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70
Q

most common surgery done for OSAHS

A

Uvulopalatopharyngoplasty
removal of the uvula and the margin of the soft palate
less successful than oral appliances

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71
Q

Sleep-breathing disorder that is ften caused by an increased sensitivity to pCO2, which leads to an unstable breathing pattern that manifests as hyperventilation alternating with apnea

A

Central sleep apnea

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72
Q

In some individuals, CPAP—particularly at high pressures—seems to induce central apnea; this condition is referred to as

A

complex sleep apnea

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73
Q

Sleep-breathing disorder that is an independent risk factor for the development of both heart failure and atrial fibrillation, possibly related to elevations in sympathetic nervous system activity that accompany this disorder

A

Central sleep apnea

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74
Q

Treatment of central sleep apnea

A
  1. treatment of the underlying cause
  2. supplemental oxygen
    No good evidence that CPAP improves health outcome if without OSAHS
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75
Q

Side effects of CPAP and its management (5)

A
  1. Nasal congestion - provide heated humidification, administer saline/ steroid nasal sprays
  2. Claustrophobia - Change mask interface, promote habituation
  3. Difficulty exhaling - Temporarily reduce pressure, provide bilevel positive airway pressure
  4. Bruised nasal ridge - Change mask interface, provide protective padding
  5. Aerophagia - Administer antacids
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76
Q

Respiratory disturbance index (RDI) is measured by

A

Number of apneas plus hypopneas plus RERAs per hour of sleep

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77
Q

Define mild, moderate, and severe OSAHS based on AHI

A

Mild OSAHS: AHI of 5–14 events/h
Moderate OSAHS: AHI of 15–29 events/h
Severe OSAHS: AHI of ≥30 events/h

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78
Q

Apnea is cessation of airflow for ______ during sleep

A

≥10 s

Accompanied by persistent respiratory effort (obstructive) and absence of respiratory effort (central)

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79
Q

Hypopnea is defined as ____ reduction in airflow for at least ____ during sleep that is accompanied by either a _____ or an ________

A

≥30%
10 s
≥3% desaturation
arousal

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80
Q

An irreversible airway dilation that involves the lung in either a focal or a diffuse manner

A

Bronchiectasis

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81
Q

3 categories of bronchiectasis and what is the most common form?

A
  • Cylindrical or tubular – the most common form
  • Varicose
  • Cystic
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82
Q

Bronchiectatic changes in a localized area of the lung

A

Focal bronchiectasis

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83
Q

Focal bronchiectasis can be caused by:

A

Intrinsic and extrinsic obstruction of the airway

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84
Q

Extrinsic cause of focal bronchiectasis:

A

Compression by adjacent lymphadenopathy or parenchymal tumor mass

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85
Q

Extrinsic cause of focal bronchiectasis (3):

A
  • Airway tumor or aspirated foreign body
  • Scarred/stenotic airway
  • Bronchial atresia
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86
Q

Widespread bronchiectatic changes throughout the lung

A

Diffuse bronchiectasis

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87
Q

Causes of bronchiectasis with more pronounced involvement of upper lung fields (2)

A

cystic fibrosis

postradiation fibrosis

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88
Q

Causes of bronchiectasis with more pronounced involvement of lower lung fields (3)

A
  1. Chronic recurrent aspiration (due to esophageal motility disorders like those in scleroderma)
  2. End-stage fibrotic lung disease
  3. Recurrent immunodeficiency-associated infection
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89
Q

Causes of bronchiectasis with more pronounced involvement of mid lung fields

A
  1. nontuberculous mycobacteria (NTM) (MAC- most common)
  2. Tracheobronchomegaly (Mounier-Kuhn syndrome)
  3. Williams-Campbell syndrome
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90
Q

Most widely cited mechanism of infectious bronchiectasis

A

Vicious cycle hypothesis

Susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree

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91
Q

Refers to dilated airways arising from parenchymal distortion as a result of lung fibrosis

A

Traction bronchiectasis

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92
Q

Most common clinical manifestation of bronchiectasis

A

Persistent productive cough with ongoing production of thick, tenacious sputum

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93
Q

Clinical features of acute exacerbations of bronchiectasis (3)

A
  • Changes in the nature of sputum production
  • Increased volume and purulence
  • Fever and new infiltrates is not be present
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94
Q

Chest radiographic finding of “tram tracks” is consistent with

A

Bronchiectasis

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95
Q

Imaging modality of choice for confirming the diagnosis of bronchiectasis

A

Chest CT scan

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96
Q

Chest CT scan findings in bronchiectasis that results from a cross-sectional area of the airway with a diameter at least 1.5 times that of the adjacent vessel

A

Signet-ring sign

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97
Q

Chest CT scan findings in bronchiectasis that results from inspissated secretions

A

“Tree-in-bud” pattern

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98
Q

Evaluation of focal bronchiectasis to exclude airway obstruction by an underlying mass or foreign body

A

Bronchoscopy

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99
Q

Aim of treatment in bronchiectasis (2)

A
  1. control of active infection
  2. improvements in secretion clearance and bronchial hygiene

to decrease the microbial load within the airways and minimize the risk of repeated infections

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100
Q

Most common organism isolated in infected bronchiectasis (2)

A

Haemophilus influenzae and P. aeruginosa

Antibiotics should be administered in acute exacerbations for minimum of 7–10 days and perhaps for as long as 14 days

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101
Q

Consensus guidelines for diagnostic criteria for true clinical infection with Non-tuberculous mycobacterium: Symptoms and radiographic findings of lung disease who have (4)

A
  • At least two sputum samples positive on culture
  • At least one bronchoalveolar lavage (BAL) fluid sample positive on culture
  • A biopsy sample displaying histopathologic features of NTM infection (e.g., granuloma or a positive stain for acid-fast bacilli) along with one positive sputum culture
  • A pleural fluid sample (or a sample from another sterile extrapulmonary site) positive on culture
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102
Q

The most common NTM pathogens in bronchiectasis

A

MAC

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103
Q

Recommended regimen for HIV-negative patients infected with macrolide-sensitive MAC

A

Macrolide + rifampin + ethambutol

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104
Q

Oral antifungal agent used in treatment of allergic bronchopulmonary aspergillosis

A

Itraconazole

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105
Q

Worse outcomes of bronchiectasis is associated with what pathogen

A

P. aeruginosa

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106
Q

Recurrent bronchiectasis is defined as

A

≥ 3 episodes per year

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107
Q

Suppressive antibiotics used in recurrent bronchiectasis

A
  1. Ciprofloxacin daily for 1-2 weeks per month
  2. Macrolide daily or 3x per week – long term macrolides of 6-12 months
  3. Aerosolized antibiotics on a rotating schedule (30 days on, 30 days off)
  4. Intermittent administration of IV antibiotics
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108
Q

Peakage of asthma

A

3 years

Many with asthma become asymptomatic during adolescence but that asthma returns in some during adult life, particularly in those with persistent symptoms and severe asthma

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109
Q

Major risk factors for asthma deaths (3)

A
  • Poorly controlled disease with frequent use of bronchodilator inhalers
  • Lack of or poor compliance with ICS therapy
  • Previous admissions to hospital with near-fatal asthma
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110
Q

The major risk factor for asthma

A

Atopy

Non-atopic individuals have a very low risk of developing asthma

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111
Q

Most common form of atopy in asthma

A

Allergic rhinitis

> 80% of asthmatic patients

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112
Q

The most consistent genetic findings that have been associated with asthma is the polymorphisms of genes on chromosome

A

5q

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113
Q

T or F. Intestinal parasites increases risk of bronchial asthma.

A

Intestinal parasite infection, such as hookworm, may reduce risk of asthma

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114
Q

T or F. Obesity is an independent risk factor for asthma, particularly in men.

A

False. In women

BMI > 30 kg/m2
May be due to mechanical factors
Also linked to pro-inflammatory adipokines and reduced anti-inflammatory adipokines that are released from fat cells

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115
Q

Percent of asthmatics that has intrinsic asthma

A

10%

Usually late-onset (adult-onset asthma)
Usually have more severe, persistent asthma

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116
Q

Intrinsic asthma is commonly associated with what upper respiratory condition

A

concomitant nasal polyps

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117
Q

Perennial allergen triggers of asthma (3)

A
  • Dermatophagoides sp. – most common
  • Cats and domestic pets
  • Cockroaches
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118
Q

Most common perennial allergen triggers

A

Dermatophagoides sp

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119
Q

Asthma that is triggered by pollen grains that are disrupted during thunderstorm

A

Thunderstorm asthma

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120
Q

Most common triggers of acute severe exacerbations of asthma

A

Upper respiratory tract virus infections

Most commonly rhinovirus, RSV, and coronavirus

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121
Q

Pharmacologic agents that may worsen asthma (3)

A

Beta adrenergic blockers
ACE inhibitors
Aspirin

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122
Q

Mechanism of exercise-induced asthma

A

Hyperventilation

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123
Q

Suggested mechanism in the premenstrual worsening of asthma

A

fall in progesterone

In severe cases, may be improved by treatment with high doses of progesterone or gonadotropin-releasing factors

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124
Q

Mechanism of stress-induced asthma

A

induce bronchoconstriction through cholinergic reflex pathways

Paradoxically, very severe stress such as bereavement usually does not worsen, and may even improve, asthma symptoms

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125
Q

Part of the airway that is predominantly involved in airway inflammation in asthma

A

Bronchi

Inflammation in the respiratory mucosa from the trachea to terminal bronchioles

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126
Q

Physiologic abnormality of asthma

A

Airway hyperresponsiveness

127
Q

May lead to irreversible narrowing of the airways in asthma

A

Airway remodelling

Early use of ICS – reduce decline in lung function

128
Q

Prodromal symptoms that may precede an asthma attack (3)

A
  • Itching under the chin
  • Discomfort between the scapulae
  • Inexplicable fear (impending doom)
129
Q

Reversibility in spirometry that is diagnostic in asthma is defined as ____ and _____ increase in FEV1 ____after an inhaled SABA or a _____trial of oral corticosteroids (prednisone or prednisolone 30-40 mg daily)

A

> 12%
200-mL
15 mins
2-4 week

130
Q

Now being used as a non-invasive test to measure eosinophilic airway inflammation

A

Fractional exhaled NO

Elevated in asthma
Reduced by ICS - may be a test of compliance with therapy

131
Q

The most effective bronchodilator

A

β2-agonist

132
Q

Adverse effects of β2-agonist (3)

A

Muscle tremor
Palpitations
Hypokalemia

133
Q

Drugs that prevent cholinergic nerve-induced bronchoconstriction and mucus secretion

A

Anticholinergic

Less effective than β2-agonist as they inhibit only the cholinergic reflex component of bronchoconstriction

134
Q

Examples of LAMA

A

tiotropium bromide

glycopyrronium

135
Q

Example of SAMA

A

ipratropium bromide

136
Q

Most common side effect of anticholinergic

A

Dry mouth (esp in elderly)

Other side effects:
Urinary retention
Glaucoma

137
Q

Drugs that inhibits phosphodiesterases in airway smooth-muscle cells

A

Theophylline

Dose required for bronchodilation commonly cause side effects
May reduce corticosteroid insensitivity in severe asthma

138
Q

A soluble salt of theophylline

A

IV aminophylline

Via slow IV infusion – in patients with severe exacerbation that are refractory to SABA

139
Q

The most effective controllers for asthma

A

Inhaled corticosteroids

Reduction in AHR is seen in chronic ICS therapy

140
Q

Local side effects of ICS that may be reduced with the use of a large- volume spacer device (2)

A

Hoarseness (dysphonia)

Oral candidiasis

141
Q

Dose of prednisone in asthma

A

30–45 mg once daily for 5–10 days

142
Q

Block cys-LT1 -receptors and provide modest clinical benefit in asthma

A

Antileukotrienes (montelukast and zafirlukast)

less effective than ICS in controlling asthma and have less effect on airway inflammation

143
Q

Less effective than ICS in controlling asthma and have less effect on airway inflammation, but are useful as an add-on therapy in some patients not controlled with low doses of ICS, although less effective than a LABA

A

Antileukotrienes

144
Q

Asthma controller drugs that appear to inhibit mast cell and sensory nerve activation and are, therefore, effective in blocking trigger-induced asthma such as EIA and allergen- and sulfur dioxide-induced symptoms

A

Cromones

Cromolyn sodium and nedocromil sodium
have relatively little benefit in the long-term control of asthma due to their short duration of action (at least four times daily by inhalation)

145
Q

Steroid-sparing therapies in asthma (5)

A 
Methotrexate
Cyclosporin A
Azathioprine
Gold
IV gamma globulin

but none of these treatments has any long-term benefit and each is associated with a relatively high risk of side effects

146
Q

a blocking antibody that neutralizes circulating IgE without binding to cell-bound IgE and, thus, inhibits IgE-mediated reactions

A

Omalizumab

subcutaneous injection every 2–4 weeks
very expensive and is only suitable for highly selected patients who are not controlled on maximal doses of inhaler therapy and have a circulating IgE within a specified range

147
Q

Anti-IL5 drugs (3)

A

Mepolizumab
Reslizumab
Benralizumab

148
Q

A bronchoscopic treatment using thermal energy to ablate airway smooth muscle in accessible bronchi

A

Bronchial Thermoplasty

149
Q

In stepwise therapy of asthma, use of a reliever medication more than ____ indicates the need for regular controller therapy

A

twice a week

150
Q

This finding in asthma is an indication of impending respiratory failure and requires immediate monitoring and therapy

A

normal or rising PCO2

PCO2 is usually low due to hyperventilation

151
Q

In treatment of acute severe asthma, a high concentration of oxygen should be given by face mask to achieve oxygen saturation of

152
Q

This medication may be given intravenously or by nebulizer in acute severe asthma, and is effective when added to inhaled β2-agonists, and is relatively well tolerated but is not routinely given.

A

Magnesium sulfate

153
Q

There are two major patterns of difficult asthma (2)

A
  • Persistent symptoms and poor lung function, despite appropriate therapy
  • Have normal or near normal lung function but intermittent, severe (sometimes life-threatening) exacerbations
154
Q

Asthma that failed to respond to a high dose of oral prednisone/prednisolone (40 mg once daily over 2 weeks), ideally with a 2-week run-in with matched placebo

A

Corticosteroid-Resistant Asthma

155
Q

Asthma subtype that show chaotic variations in lung function despite taking appropriate therapy

A

Brittle Asthma

156
Q

Asthma subtype that show a persistent pattern of variability and may require OCS or, at times, continuous infusion of β2-agonists

A

Type 1 brittle asthma

157
Q

Asthma subtype that show generally normal or near-normal lung function but precipitous, unpredictable falls in lung function that may result in death

A

Type 2 brittle asthma

difficult to manage as they do not respond well to corticosteroids, and the worsening of asthma does not reverse well with inhaled bronchodilators

158
Q

The most effective therapy in type 2 brittle asthma

A

subcutaneous epinephrine

suggests that the worsening is likely to be a localized airway anaphylactic reaction with edema

159
Q

T or F. In management of aspirin-sensitive asthma, all nonselective COX inhibitors should be avoided, but selective COX2 inhibitors are safe to use when an anti-inflammatory analgesic is needed

160
Q

Approximately ______ of asthmatic patients who are pregnant improve during the course of a pregnancy, ______ deteriorate, and _________ are unchanged

161
Q

Better OCS to be used in asthma in pregnancy

A

Prednisone

it is better to use prednisone rather than prednisolone as it cannot be converted to the active prednisolone by the fetal liver, thus protecting the fetus from systemic effects

162
Q

Some patients report a temporary worsening of asthma when they first stop smoking, possibly due to the

A

loss of the bronchodilating effect of NO in cigarette smoke

163
Q

Asthmatic patients with FEV1 ____ of their normal levels should also be given a boost of OCS prior to surgery.

164
Q

On of the aims of asthma therapy is the peak expiratory flow circadian variation of

165
Q

Define controlled asthma based on:

Daytime symptoms
Limitation of activities
Nocturnal symptoms/awakening
Need for reliever/rescue treatment
Lung function (PEF or FEV1)
A 
Daytime symptoms: None (≤2/week) 
Limitation of activities: None
Nocturnal symptoms/awakening: None
Need for reliever/rescue treatment: None (≤2/week) 
Lung function (PEF or FEV1): None
166
Q

Define partly-controlled asthma based on:

Daytime symptoms
Limitation of activities
Nocturnal symptoms/awakening
Need for reliever/rescue treatment
Lung function (PEF or FEV1)
A

Daytime symptoms: >2/week)
Limitation of activities: Any
Nocturnal symptoms/awakening: Any
Need for reliever/rescue treatment: >2/week
Lung function (PEF or FEV1): <80% predicted or personal best

167
Q

Define uncontrolled asthma

A

3 or more features of partly controlled asthma

168
Q

Pulmonary hypertension is defined as an elevation in pulmonary arterial pressures (mean pulmonary artery pressure [PAP] _____ or an estimated systolic PAP________)

A

> 22 mmHg

>36 mmHg

169
Q

The most common cause of death in pulmonary arterial hypertension

A

Decompensated right heart failure

170
Q

More common symptoms of PH (2)

A

dyspnea and/or fatigue

Less common symptoms: edema, chest pain, presyncope, and syncope

171
Q

The most important initial screening test of pulmonary hypertension

A

Echocardiogram with bubble study

172
Q

The gold standard for diagnosis and assessment of disease severity

A

Invasive hemodynamic monitoring

173
Q

In patients suspected with PH with normal echocardiogram but with unexplained dyspnea or hypoxemia, it is reasonable to proceed to

A

right heart catheterization (RHC) for definitive diagnosis

If the patient has a reasonable functional capacity, a cardiopulmonary exercise test may help to identify a true physiologic limitation as well as differentiate between cardiac and pulmonary causes of dyspnea

174
Q

Isolated reduction in diffusing capacity of the lungs for carbon monoxide (DLCO) in pulmonary function test is a classing finding in

A

Pulmonary arterial hypertension

175
Q

Test don in PH patients that is important to evaluate the degree of exertional hypoxemia and limitation, and to monitor progression and response to therapy

A

6-minute walk test

176
Q

T or F. Since-breathing disorders is an important cause of mild PH, sleep study must be done to patients suspected to have PH

A

False. Sleep study is generally necessary only when indicated by the patient’s history

177
Q

Remains the gold standard both to establish the diagnosis of PH and to guide selection of appropriate medical therapy

A

RHC with pulmonary vasodilator testing

178
Q

The definition of precapillary PH or PAH requires (3):

A
  • An increased mean PAP (mPAP >25 mmHg)
  • A pulmonary capillary wedge pressure (PCWP), left atrial pressure, or left ventricular end-diastolic pressure (LVEDP) ≤15 mmHg
  • PVR >3 Wood units
179
Q

Passive post capillary PH is defined as (2)

A
  • PCWP ≥15 mmHg

* Transpulmonary gradient <12 mmHg

180
Q

Reactive post capillary PH is defined as (3)

A
  • PCWP ≥15 mmHg
  • Transpulmonary gradient >12 mmHg
  • Incresed PVR
181
Q

Preferred for vasodilator testing in right heart catheterization

A

Vasodilators with a short duration of action (i.e. inhaled nitric oxide (NO), or inhaled epoprostenol)

182
Q

Positive response for vasodilator testing during RHC

A

a decrease in mPAP by ≥10 mmHg to an absolute level ≤40 mmHg without a decrease in CO

183
Q

Treatment that may be given to PH patents with positive response to RHC with pulmonary vasodilator testing

A

long-term treatment with calcium channel blockers (CCB)

184
Q

WHO Group I PH

A

Pulmonary arterial hypertension – rare cause

185
Q

PAH is defined as a ________ in resting mean pulmonary arterial pressure (mPAP) ________ , PVR________, and PCWP or LVEDP of _________based on a RHC

A

sustained elevation
≥25 mmHg
> 240 dyne-s/cm5
≤15 mmHg

186
Q

Rare infectious cause of PAH

A

HIV

  • An important cause of mortality in the HIV-infected population
  • No correlation between the stage of HIV infection and the development of PAH
187
Q

Only connective tissue diseases associated with PAH

A

Systemic sclerosis

Patients who eventually develop scleroderma-associated PAH tend to be older at the time of scleroderma diagnosis

188
Q

Systemic sclerosis subtype that is most commonly associated with PAH

A

Cutaneous scleroderma

189
Q

WHO Group II PH

A

Pulmonary hypertension associated with left heart disease

190
Q

Which form of HF that has higher overall risk of PH

191
Q

T or F. PH portends a poor prognosis in all forms of HF

192
Q

Hall mark of WHO Group II PH

A

Elevated left atrial pressure with resulting pulmonary venous hypertension

193
Q

WHO Group III PH

A

Pulmonary hypertension associated with lung disease

194
Q

the second most common cause of PH

A

Intrinsic lung disease

195
Q

The most studied form of interstitial lung disease associated with PH

A

Idiopathic pulmonary fibrosis

196
Q

WHO Group IV PH

A

PH with chronic thromboembolic disease

197
Q

Important and often the dominant factor in WHO Group IV PH

A

Obstruction of the proximal pulmonary vasculature

198
Q

Infectious cause of PH which is one of the most common cause globally

A

Schistosomiasis

Occurs in the setting of hepatosplenic disease and portal hypertension

199
Q

T or F. Without treatment PAH is invariably fatal

200
Q

Drugs that addresses the imbalance of arachidonic acid metabolites with reduced prostacyclin levels and increased thromboxane A2 production in PAH

A

Prostanoids

201
Q

The first prostanoid available for the management of PAH

A

Epoprostenol

  • Continuous intravenous infusion
  • Improves functional capacity and survival in PAH
202
Q

Increase cyclic guanosine monophosphate (cGMP) levels and activate cGMP-dependent signaling pathways that also mediate vasodilation and platelet inhibition, and augments the pulmonary hemodynamic and functional capacity benefits of prostanoids in PAH

A

Phosphodiesterase-5 (PDE5) inhibitors (e.g., sildenafil)

203
Q

An oral nonprostanoid diphenylpyrazine derivative used in the treatment of PAH that binds the prostaglandin I2 (IP) receptor with high affinity

204
Q

Non-selective ET-1 receptor antagonists that improves hemodynamics and exercise capacity and delays clinical worsening of PAH

205
Q

A selective ET-A receptor antagonist used in treatment of PH

A

Ambrisentan

206
Q

Drug used in PH that prolong the vasodilatory effect of NO, especially within the pulmonary arterial bed where high concentrations of cGMP are found

A

cGMP phosphodiesterase type 5 (PDE5) inhibitors

207
Q

Two PDE5 inhibitors used for the treatment of PAH:

A
  • Sildenafil

* Tadalafil

208
Q

A clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure

209
Q

2 most common cause of ARDS

A

Pneumonia and sepsis

Other causes:

  1. Aspiration of gastric contents
  2. Trauma
  3. Multiple transfusion
  4. Drug overdose
210
Q

Most common trauma injury that causes ARDS (3)

A
  1. Pulmonary contusion
  2. Multiple bone fractures
  3. Chest wall trauma / flail chest

Head trauma, near-drowning, toxic inhalation, and burns – rare causes

211
Q

Clinical variables associated with the development of ARDS (5)

A
  1. Older age
  2. Chronic alcohol abuse
  3. Metabolic acidosis
  4. Pancreatitis
  5. Severity of critical illness
212
Q

Trauma patients with APACHE II score of ___ have 2.5-fold increased risk for ARDS

213
Q

3 phases of ARDS

A
  1. Exudative phase
  2. Proliferative phase
  3. Fibrotic phase
214
Q

Phase of ARDS wherein edema fluid that is rich in protein accumulates in the interstitial and alveolar spaces

A

Exudative phase

215
Q

Phase of ARDS with neutrophil as the predominant cells

A

Exudative phase

216
Q

Phase of ARDS wherein condensed plasma proteins aggregate in the air spaces with cellular debris and dysfunctional pulmonary surfactant to form hyaline membrane whorls

A

Exudative phase

217
Q

Prominent in early ARDS: hypocapnia or hypercapnia

A

Hypercapnia

218
Q

Exudative phase of ARDS occur in the _____ days of illness

A

1st 7 days

219
Q

ARDS patient experience onset of respiratory symptoms usually within ____ after initial insult

A

12-36 hours

220
Q

12-36 hours

221
Q

Proliferative phase of ARDS occur in the day _____ of illness

A

Day 7 to day 21

Most patients recover rapidly and are liberated from mechanical ventilation

222
Q

Phase of ARDS wherein some patients develop progressive lung injury and early changes of pulmonary fibrosis

A

Proliferative phase

223
Q

Histologically, 1st signs of resolution are seen in this phase of ARDS

A

Proliferative phase

1st signs of resolution

  1. Initiation of lung repair
  2. Organization of alveolar exudates
  3. Shift from neutrophil to lymphocyte-predominant pulmonary infiltrates
224
Q

Phase of ARDS with lymphocyte as its predominant cell

A

Proliferative phase

225
Q

T or F. All patient with ARDS enter the 3rd phase

A

False. Some patients enter fibrotic phase that may require long-term support on mechanical ventilators and/or supplemental oxygen

226
Q

Phase of ARDS characterized by arked disruption of acinar architecture resulting to emphysema-like changes with large bullae

227
Q

2 principal mechanism of ventilator-induced lung injury:

A
  1. “Volutrauma” from repeated alveolar overdistention from excess tidal volume
  2. “Atelectrauma” from recurrent alveolar collapse

Because compliance differs in affected versus more “normal” areas of the lung, attempts to fully inflate the consolidated lung may lead to overdistention of and injury to the more normal areas

228
Q

Clinicians must empirically measure the “best PEEP” at the bed side to determine the optimal settings that best promotes (3)

A
  1. alveolar recruitment
  2. minimizes alveolar overdistention and hemodynamic instability
  3. Provides adequate Pao2 while minimizing Fio2
229
Q

This position may improve arterial oxygenation in ARDS

A

Prone positioning

230
Q

Strategy in mechanical ventilation that transiently increase PEEP to high levels to “recruit” atelectatic lung can increase oxygenation

A

Recruitment maneuvers

231
Q

Rescue therapy for ARDS that improve mortality

A

Lung-replacement therapy with extracorporeal membrane oxygenation (ECMO)

Improve mortality for patients with ARDS in the United Kingdom who were referred to an ECMO center

232
Q

T or F. Fluid restriction therapy and diuretics are important aspects in ARDS management

233
Q

This drugs may be given to improve the patient-ventilator synchrony in ARDS

A

Sedative
Neuromuscular blockade

In a multicenter, randomized, placebo-controlled trial of early neuromuscular blockade (with cisatracurium besylate) for 48 h, patients with severe ARDS had increased survival and ventilator-free days without increasing ICU-acquired paresis

234
Q

T or F. Glucocorticoid is routinely given in severe ARDS

235
Q

According tp Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure (LUNG SAFE) trial, mortality rates of mild, moderate and severe ARDS are:

A
  • 34.9% for mild ARDS
  • 40.3% for moderate ARDS
  • 46.1% with severe ARDS
236
Q

Mortality in ARDS is attributable to (2)

A
  1. Sepsis

2. Nonpulmonary organ failure

237
Q

Major risk factors for ARDS mortality (4)

A
  1. Advanced age
  2. Preexisting organ dysfunction from chronic medical illness
  3. Direct lung injury – nearly twice as likely to die as those with indirect causes of lung injury
  4. Severity of ARDS
238
Q

In ARDS, patients usually recover maximal lung function within

239
Q

Recovery of lung function post ARDS is strongly associated with the _________

A

extent of lung injury in early ARDS

240
Q

Direct lung injury that causes ARDS (5)

A
  1. Pneumonia
  2. Aspiration of gastric contents
  3. Pulmonary contusion
  4. Near-drowning
  5. Toxic inhalation injury
241
Q

Indirect lung injury that causes ARDS (6)

A
  1. Sepsis
  2. Severe trauma
  3. Multiple transfusions
  4. Drug overdose
  5. Pancreatitis
  6. Postcardiopulmonary bypass
242
Q

Mild, moderate and severe ARDS are defined as

A

Mild: Pao2/Fio2 200 mmHg - 300 mmHg
Moderate: Pao2/Fio2100 mmHg - 200 mmHg
Severe: Pao2/Fio2 ≤ 100 mmHg

243
Q

Class A recommendation for management of ARDS

A

Low tidal volume

244
Q

Class B recommendations for management of ARDS (5)

A
  1. Minimized left atrial filling pressures
  2. High-PEEP or “open lung”
  3. Prone position
  4. ECMO
  5. Early neuromuscular blockade
245
Q 
Goals and limits in ARDS based on:
Tidal volume
Plateau pressure
RR
FiO2
SpO2
pH
MAP
A 
Tidal volume ≤6 ml/kg
Plateau pressure ≤30 cmH2O
RR ≤ 35 bpm
FiO2 ≤ 0.6
SpO2 ≤ 88-95
pH ≥7.30
MAP ≥65 mmHg
246
Q

Most common way for microorganism to gain access to the lower respiratory tract

A

Aspiration from the oropharynx

247
Q

Mechanical host defense that traps microbes on the airway lining

A

Branching architecture of the tracheobronchial tree

248
Q

Extremely efficient at clearing and killing pathogens in the respiratory tract

A

Alveolar macrophages

Assisted by proteins that are produced by the alveolar epithelial cells (e.g., surfactant proteins A and D) - have intrinsic opsonizing properties or antibacterial or antiviral activity

249
Q

The two most likely sources of an altered alveolar microbiota

A
  1. Viral upper respiratory tract infections for CAP

2. Antibiotic therapy for HAP/VAP

250
Q

Phase of pneumonia characterized by presence of a proteinaceous exudate—and often of bacteria—in the alveoli

A

Edema

1st phase
Rarely evident in clinical or autopsy specimens

251
Q

Phase of pneumonia characterized by presence of erythrocytes in the cellular intra-alveolar exudate

A

Red hepatization

252
Q

Phase of pneumonia characterized by neutrophil influx

A

Red hepatization

Bacteria are occasionally seen in pathologic specimens

253
Q

Phase of pneumonia characterized by lysis and degradation of the erythrocytes and no new erythrocytes are extravasating

A

Gray hepatisation

254
Q

Phase of pneumonia characterized by abundance of fibrin deposition

A

Gray hepatization

255
Q

Predominant cell in gray hepatization

A

Neutrophil

256
Q

Phase of pneumonia characterized by disappearance of bacteria and successful containment of the infection and improvement in gas exchange

A

Gray hepatization

257
Q

Predominant cell in resolution phase of pneumonia

A

macrophage

258
Q

Phase of pneumonia characterized by clearance of the debris of neutrophils, bacteria, and fibrin

A

Resolution

259
Q

Phase of pneumonia that is described best for lobar pneumococcal pneumonia and may not apply to pneumonia of all etiologies, especially viral or Pneumocystis pneumonia

A

Resolution

260
Q

Most common pattern in nosocomial pneumonia

A

Bronchopneumonia pattern

Because of the microaspiration mechanism

261
Q

Most common pattern in bacterial CAP

A

Lobar pattern

262
Q

Most common cause of CAP

A

Streptococcus pneumoniae

263
Q

Atypical bacteria causing pneumonia (3)

A
  1. Mycoplasma pneumonia
  2. Chlamydia pneumonia
  3. Legionella
264
Q

Most common viruses causing CAP (3)

A
  1. Influenza
  2. Parainfluenza
  3. Respiratory syncytial viruses
265
Q

May cause necrotizing pneumonia (2)

A

S. aureus pneumonia
P. aeruginosa

Complicate influenza infection

266
Q

Risk factors for CAP (5)

A
  1. Alcoholism
  2. Asthma
  3. Immunosuppression
  4. Institutionalization
  5. Age of ≥70 years
267
Q

Risk factors for pneumococcal pneumonia (8)

A
  1. Dementia
  2. Seizure disorders
  3. Heart failure
  4. Cerebrovascular disease
  5. Alcoholism
  6. Tobacco smoking
  7. Chronic obstructive pulmonary disease (COPD)
  8. HIV infection
268
Q

Risk factors for CA-MRSA pneumonia

A

Skin colonization or infection with CA-MRSA

269
Q

Risk factors for Enterobacteriaceae-casued pneumonia (5)

A
  1. Recently been hospitalized
  2. Received antibiotic therapy
  3. Alcoholism
  4. Heart failure
  5. Renal failure
270
Q

Risk factors for P. aeruginosa pneumonia

A

Severe structural lung disease (bronchiectasis, cystic fibrosis, or severe COPD)

271
Q

Risk factors for Legionella pneumonia (8)

A
  1. Diabetes
  2. Hematologic malignancy
  3. Cancer
  4. Severe renal disease
  5. HIV infection
  6. Smoking
  7. Male gender
  8. Recent hotel stay or ship cruise
272
Q

Gross hemoptysis is suggestive of what pneumonia

A

CA-MRSA pneumonia

273
Q

Chest radiography finding of pneumatoceles is suggestive of what cause of pneumonia

274
Q

To be adequate for culture, a sputum sample must have ___ neutrophils and ____ squamous epithelial cells per low-power field

275
Q

Main purpose of sputum GS

A

ensure that a sample is suitable for culture

276
Q

T or F. Blood cultures must be done in all patients with CAP

A

False.

Certain high risk patients must have blood cultures:

  1. Neutropenia
  2. Asplenia
  3. Complement deficiencies
  4. Chronic liver disease
  5. Severe CAP
277
Q

Urinary antigen tests detects what antigen that may be causative of pneumonia (2)

A

Pneumococcal
Legionella (serogroup 1)

Both tests can detect antigen even after the initiation of appropriate antibiotic therapy

278
Q

Accounts for most community-acquired cases of Legionnaires’ disease

A

Legionella pneumophila serogroup 1

279
Q

A 20-variable prognostic model used to identify patients at low risk of dying

A

Pneumonia Severity Index (PSI)

Age, coexisting illness, and abnormal physical and laboratory findings

Routine use of the PSI results in lower admission rates for class 1 and class 2 patients

Patients in class 3 could ideally be admitted to an observation unit until a further decision

280
Q

Mortality rates of the 5 classes of Pneumonia Severity Index (PSI)

A
  1. Class 1: 0.1%
  2. Class 2: 0.6%
  3. Class 3: 2.8%
  4. Class 4: 8.2%
  5. Class 5: 29.2%
281
Q

A 5-variable severity-of-illness scoring for pneumonia

A

CURB-65 criteria

282
Q

5 variables of CURB-65 criteria

A
  1. Confusion (C)
  2. Urea >7 mmol/L (U)
  3. Respiratory rate ≥30/min (R)
  4. Blood pressure, systolic ≤90 mmHg or diastolic ≤60 mmHg (B)
  5. Age ≥65 years
283
Q

CURB-65 score that can be treated outside the hospital

A

Score 0

30-day mortality rate is 1.5%

284
Q

CURB-65 score indicating that patient should be hospitalized unless the score is entirely or in part attributable to an age of ≥65 years

A

Score of 1 or 2

285
Q

CURB-65 score may require ICU admission

286
Q

Mortality rate of CURB-65 score of ≥3

287
Q

Minimal inhibitory concentration (MIC) cutoffs for penicillin for susceptible, intermediate, and resistant

A
  • ≤2 μg/mL for susceptible
  • > 2–4 μg/mL for intermediate
  • ≥8 μg/mL for resistant
288
Q

Isolates resistant to drugs from ____ antimicrobial classes with different mechanisms of action are considered MDR strains

A

three or more

289
Q

The most important risk factor for antibiotic-resistant pneumococcal infection is

A

use of a specific antibiotic within the previous 3 months

290
Q

Most important distinction of CA-MRSA from the hospital-acquired MRSA

A

Carry genes for superantigens

Enterotoxins B and C and Panton-Valentine leukocidin, a membrane-tropic toxin that can create cytolytic pores in polymorphonuclear neutrophils, monocytes, and macrophages

291
Q

Found to be superior to Ceftriaxone as the β-lactam component of IV empirical treatment of CAP in hospitalized patients in PORT risk class III or IV who have not received prior antibiotics

A

Ceftaroline

292
Q

Pneumonia patients slow to respond to therapy should be reevaluated at about

A

day 3

sooner if their condition is worsening rather than simply not improving

293
Q

Indication for complete drainage by chest tube of pleural effusion (4)

A
  1. pH of <7
  2. Glucose level of <2.2 mmol/L
  3. Lactate dehydrogenase concentration of >1000 U/L
  4. Bacteria are seen or cultured
294
Q

Chest radiographic abnormalities of pneumonia may resolve at how many weeks?

A

4-12 weeks

295
Q

Outpatient mortality rate of pneumonia

296
Q

Inpatient mortality rate of pneumonia

297
Q

Non-MDR pathogens predominate if VAP develops in the first ____ of the hospital stay

A

5–7 days

298
Q

The most obvious risk factor for VAP

A

ET tube

May prevent large-volume aspiration, but microaspiration is exacerbated by secretions pooling above the cuff

299
Q

Diagnostic threshold of ETA sample for VAP

A

10^6 cfu/mL

300
Q

Diagnostic threshold of protected specimen brush method for VAP

A

10^3 cfu/mL

301
Q

Achilles heel of Quantitative-Culture Approach of diagnosing VAP

A

The effect of antibiotic therapy

With sensitive microorganisms, a single antibiotic dose can reduce colony counts below the diagnostic threshold

302
Q

The major risk factor for infection with MRSA and extended-spectrum β-lactamase–positive strains

A

Frequent use of β-lactam drugs, especially cephalosporins

303
Q

Etiologic agents of VAP that are intrinsically resistant to many of the empirical antibiotic regimens employed (3)

A
  1. Acinetobacter species
  2. Stenotrophomonas maltophilia
  3. Burkholderia cepacia
304
Q

There is lower incidence of atypical pathogens in VAP except for

A

Legionella

305
Q

Major complication of VAP

A

Prolongation of mechanical ventilation

306
Q

Mortality rate of VAP

307
Q

Pneumonia caused by this pathogen is simply a marker for a patient whose immune system is so compromised that death is almost inevitable

A

S. maltophilia

308
Q

Risk factors for pneumonia caused by MDR gram-negative bacteria and MRSA (7)

A
  1. Hospitalization ≥2 days in previous 90 days
  2. Use of antibiotics in previous 90 days
  3. Immunosuppression
  4. Nonambulatory status
  5. Tube feedings
  6. Gastric acid suppression
  7. Severe COPD or bronchiectasis
309
Q

Risk factors for pneumonia caused by nosocomial MRSA (6)

A
  1. Hospitalization ≥ 2 days in previous 90 days
  2. Use of antibiotics in previous 90 days
  3. Chronic hemodialysis in previous 30 days
  4. Documented prior MRSA colonization
  5. Congestive heart failure
  6. Gastric acid suppression
310
Q

Risk factors for pneumonia caused by CA-MRSA (7)

A
  1. Cavitary infiltrate or necrosis
  2. Gross hemoptysis
  3. Neutropenia
  4. Erythematous rash
  5. Concurrent influenza
  6. Young, previously healthy status
  7. Summer-month onset
311
Q

Possible cause of CAP when there is history of exposure to bats

A

H. capsulatum

312
Q

Possible cause of CAP when there is history of exposure to birds (2)

A
  1. H. capsulatum

2. Chlamydia psittaci

313
Q

Possible cause of CAP when there is history of exposure to rabbits

A

Francisella tularensis

314
Q

Possible cause of CAP when there is history of exposure to sheep, goats, parturient cats

A

Coxiella burnetii

PSBIM (12 decks)

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