PULMONOLOGY Flashcards
(314 cards)
1
Q
Most common site of bleeding in hemoptysis
A
Bronchi or medium-sized airways
2
Q
Unique feature of the lung that predisposes to hemoptysis of varied severity
A
Dual blood supply
3
Q
Dual blood supply of the lung
A
Pulmonary circulation
Bronchial circulation
4
Q
Most common cause of blood-tinged sputum and small-volume hemoptysis
A
Viral bronchitis
5
Q
Leading cause of massive hemoptysis and subsequent death
A
Bronchiectasis
6
Q
Most common cause of hemoptysis worldwide
A
Tuberculosis
7
Q
Most frequent source of bleeding in the hemoptysis in tuberculosis
A
Cavitary disease
8
Q
Rare cause of hemoptysis where there is erosion of a pulmonary artery aneurysm into the preexisting cavity
A
Rasmussen’s aneurysm
9
Q
A disease that mimic tuberculosis and acquired from raw crayfish ingestion
A
Paragonomiasis
10
Q
Cyclical hemoptysis
A
Catamenial hemoptysis
11
Q
Cause of catamenial hemoptysis
A
Pulmonary endometriosis
12
Q
First step in evaluating hemoptysis
A
Determine the amount or severity of bleeding
13
Q
Definition of massive hemoptysis
A
Blood loss of 400 mL in 24 hours or 100-150 mL expectorated at one time
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
15
Q
3 simultaneous goals if with massive hemoptysis:
A
Protect the non-bleeding lung
Locate the site of bleeding
Control the bleeding
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
17
Q
Procedure of choice for control of massive hemoptysis
A
Bronchial artery embolization
18
Q
Complication of bronchial artery embolization
A
embolization of the anterior spinal artery
19
Q
Ideal candidate for surgical resection in patients with hemoptysis:
A
Localized disease but otherwise normal lung parenchyma
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)
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
22
Q
Etiology of primary lung abscess
A
Anaerobic bacteria / aspiration
23
Q
Duration of acute lung abscess and chronic lung abscess
A
<4-6 weeks
> 6 weeks
24
Q
Major risk factor for primary lung abscesses
A
Aspiration
25
Lung abscesses also arise from septic emboli from what endocarditis?
Tricuspid valve endocarditis
26
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
Lemierre’s syndrome
27
Most common locations of primary lung abscess
Posterior upper lobes and superior lower lobes – dependent segments
28
Which lung is usually affected in lung abscess?
Right lung (Right mainstem bronchus is less angulated)
29
With foul-smelling breath, sputum, or empyema and essentially diagnostic of an anaerobic lung abscess
Putrid lung abscess
30
Most common organisms causing secondary lung abscess
Pseudomonas aeruginosa and other gram-negative rods
31
More fulminant course of lung abscess with high fever is usually caused by
S. aureus
32
DOC for primary lung abscess
Clindamycin 600 mg q8hrs and IV β-lactam/β-lactamase combination
33
Duration of treatment of primary lung abscess
3–4 weeks to as long as 14 weeks
34
Size of lung abscess that is less likely to respond to antibiotic therapy without additional interventions
>6-8 cm
35
Poor prognostic factors for lung abscess (5)
```
Age of >60
Presence of aerobic bacteria
Sepsis at presentation
Symptom duration of >8 weeks
Abscess size of >6 cm
```
36
Where is the cough center located?
nucleus tractus solitarius
37
Maximal expiratory pressure at the mouth is called:
Peak expiratory flow
38
Surrogate marker for cough strength
Peak expiratory flow
39
Duration of acute cough
< 3 weeks
40
Duration of subacute cough
3-8 weeks
41
Duration of chronic cough
> 8 weeks
42
Kind of cough that lingers for >2 months following one or more respiratory tract infections
Post-bronchitic cough
43
How many % of patients taking ACE inhibitors has persistent cough?
5-30%
44
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?
1 month
45
Most potent cough suppressants
Narcotic cough suppressants (codeine and hydrocodone)
46
2 sleep-related breathing disorders and what is more common
1. Obstructive sleep apnea/hypopnea syndrome (OSAHS) – more common
2. Central sleep apnea (CSA)
47
Definition of OSAHS
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
48
Apnea-hypopnea index (AHI) calculated as
the number of episodes divided by the number of hours of sleep
49
Apnea-hypopnea index that can be considered as OSAHS even if with no symptoms
> 15 episodes/h
50
OSAHS severity is based on (5)
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
51
Pharyngeal airway has no bone or cartilage, hence, airway patency is dependent on the stabilizing influence of the
pharyngeal dilator muscles
52
Most common site of airway collapse in OSAHS
Soft palate
Other sites:
1. Tongue base
2. Lateral pharyngeal walls
3. Epiglottis
53
OSAHS may be most severe during what stage of sleep and what position?
REM (rapid eye movement) sleep - neuromuscular output to the skeletal muscles is particularly low
Supine position
54
REM (rapid eye movement) sleep - neuromuscular output to the skeletal muscles is particularly low
Supine position
1. Ventilatory sensitivity
2. Arousal threshold
3. Neuromuscular responses to CO2
55
Major risk factors for OSAHS (2):
1. Obesity
2. Male sex
Absence of obesity does not exclude this diagnosis
56
10% weight gain is associated with a ____ increase in apnea-hypopnea index
>30%
57
Reasons why male sex is a risk factor for OSAHS (2)
1. Android patterns of obesity
| 2. Relatively greater pharyngeal length
58
Additional risk factors for OSAHS aside from male sex and obesity (6)
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
59
The most common complaint of OSAHS
Snoring
however, its absence does not exclude the diagnosis
60
Symptoms reflecting termination of individual apneas with abrupt airway opening in OSAHS
Gasping
| Snorting
61
Generally distinguishes OSAHS from paroxysmal nocturnal dyspnea, nocturnal asthma, and acid reflux with laryngospasm
Absence of dyspnea
62
The most common daytime symptom of OSAHS is
excessive sleepiness
many women preferentially report fatigue rather than sleepiness
63
The gold standard for diagnosis of OSAHS is
```
overnight polysomnogram (PSG)
A negative in-laboratory PSG usually rules out OSAHS
```
64
The key physiological information collected during a sleep study for OSAHS assessment includes (4)
1. measurement of breathing (changes in airflow, respiratory excursion)
2. oxygenation
3. body position
4. cardiac rhythm
65
Measure in sleep study that includes the number of respiratory effort-related arousals in addition to the number of apneas plus hypopneas
respiratory disturbance index
66
Arousal index in sleep study is measured by
frequency of cortical micro-arousals or awakenings per sleep hour
67
Overnight blood pressure monitoring in OSAHS often displays what pattern
“non-dipping” pattern
absence of the typical 10-mmHg fall of blood pressure during sleep compared to wakefulness
68
It is the most common medical cause of daytime sleepiness and negatively influences quality of life
OSAHS
69
the standard medical therapy with the highest level of evidence for efficacy for OSAHS
CPAP
Other management:
Oral appliances – for mild OSAHS
Upper airway surgery
Bariatric surgery
70
most common surgery done for OSAHS
Uvulopalatopharyngoplasty
removal of the uvula and the margin of the soft palate
less successful than oral appliances
71
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
Central sleep apnea
72
In some individuals, CPAP—particularly at high pressures—seems to induce central apnea; this condition is referred to as
complex sleep apnea
73
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
Central sleep apnea
74
Treatment of central sleep apnea
1. treatment of the underlying cause
2. supplemental oxygen
No good evidence that CPAP improves health outcome if without OSAHS
75
Side effects of CPAP and its management (5)
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
76
Respiratory disturbance index (RDI) is measured by
Number of apneas plus hypopneas plus RERAs per hour of sleep
77
Define mild, moderate, and severe OSAHS based on AHI
Mild OSAHS: AHI of 5–14 events/h
Moderate OSAHS: AHI of 15–29 events/h
Severe OSAHS: AHI of ≥30 events/h
78
Apnea is cessation of airflow for ______ during sleep
≥10 s
| Accompanied by persistent respiratory effort (obstructive) and absence of respiratory effort (central)
79
Hypopnea is defined as ____ reduction in airflow for at least ____ during sleep that is accompanied by either a _____ or an ________
≥30%
10 s
≥3% desaturation
arousal
80
An irreversible airway dilation that involves the lung in either a focal or a diffuse manner
Bronchiectasis
81
3 categories of bronchiectasis and what is the most common form?
* Cylindrical or tubular – the most common form
* Varicose
* Cystic
82
Bronchiectatic changes in a localized area of the lung
Focal bronchiectasis
83
Focal bronchiectasis can be caused by:
Intrinsic and extrinsic obstruction of the airway
84
Extrinsic cause of focal bronchiectasis:
Compression by adjacent lymphadenopathy or parenchymal tumor mass
85
Extrinsic cause of focal bronchiectasis (3):
* Airway tumor or aspirated foreign body
* Scarred/stenotic airway
* Bronchial atresia
86
Widespread bronchiectatic changes throughout the lung
Diffuse bronchiectasis
87
Causes of bronchiectasis with more pronounced involvement of upper lung fields (2)
cystic fibrosis
| postradiation fibrosis
88
Causes of bronchiectasis with more pronounced involvement of lower lung fields (3)
1. Chronic recurrent aspiration (due to esophageal motility disorders like those in scleroderma)
2. End-stage fibrotic lung disease
3. Recurrent immunodeficiency-associated infection
89
Causes of bronchiectasis with more pronounced involvement of mid lung fields
1. nontuberculous mycobacteria (NTM) (MAC- most common)
2. Tracheobronchomegaly (Mounier-Kuhn syndrome)
3. Williams-Campbell syndrome
90
Most widely cited mechanism of infectious bronchiectasis
Vicious cycle hypothesis
Susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree
91
Refers to dilated airways arising from parenchymal distortion as a result of lung fibrosis
Traction bronchiectasis
92
Most common clinical manifestation of bronchiectasis
Persistent productive cough with ongoing production of thick, tenacious sputum
93
Clinical features of acute exacerbations of bronchiectasis (3)
* Changes in the nature of sputum production
* Increased volume and purulence
* Fever and new infiltrates is not be present
94
Chest radiographic finding of “tram tracks” is consistent with
Bronchiectasis
95
Imaging modality of choice for confirming the diagnosis of bronchiectasis
Chest CT scan
96
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
Signet-ring sign
97
Chest CT scan findings in bronchiectasis that results from inspissated secretions
“Tree-in-bud” pattern
98
Evaluation of focal bronchiectasis to exclude airway obstruction by an underlying mass or foreign body
Bronchoscopy
99
Aim of treatment in bronchiectasis (2)
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
100
Most common organism isolated in infected bronchiectasis (2)
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
101
Consensus guidelines for diagnostic criteria for true clinical infection with Non-tuberculous mycobacterium: Symptoms and radiographic findings of lung disease who have (4)
* 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
102
The most common NTM pathogens in bronchiectasis
MAC
103
Recommended regimen for HIV-negative patients infected with macrolide-sensitive MAC
Macrolide + rifampin + ethambutol
104
Oral antifungal agent used in treatment of allergic bronchopulmonary aspergillosis
Itraconazole
105
Worse outcomes of bronchiectasis is associated with what pathogen
P. aeruginosa
106
Recurrent bronchiectasis is defined as
≥ 3 episodes per year
107
Suppressive antibiotics used in recurrent bronchiectasis
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
108
Peakage of asthma
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
109
Major risk factors for asthma deaths (3)
* 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
110
The major risk factor for asthma
Atopy
Non-atopic individuals have a very low risk of developing asthma
111
Most common form of atopy in asthma
Allergic rhinitis
> 80% of asthmatic patients
112
The most consistent genetic findings that have been associated with asthma is the polymorphisms of genes on chromosome
5q
113
T or F. Intestinal parasites increases risk of bronchial asthma.
Intestinal parasite infection, such as hookworm, may reduce risk of asthma
114
T or F. Obesity is an independent risk factor for asthma, particularly in men.
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
115
Percent of asthmatics that has intrinsic asthma
10%
Usually late-onset (adult-onset asthma)
Usually have more severe, persistent asthma
116
Intrinsic asthma is commonly associated with what upper respiratory condition
concomitant nasal polyps
117
Perennial allergen triggers of asthma (3)
* Dermatophagoides sp. – most common
* Cats and domestic pets
* Cockroaches
118
Most common perennial allergen triggers
Dermatophagoides sp
119
Asthma that is triggered by pollen grains that are disrupted during thunderstorm
Thunderstorm asthma
120
Most common triggers of acute severe exacerbations of asthma
Upper respiratory tract virus infections
Most commonly rhinovirus, RSV, and coronavirus
121
Pharmacologic agents that may worsen asthma (3)
Beta adrenergic blockers
ACE inhibitors
Aspirin
122
Mechanism of exercise-induced asthma
Hyperventilation
123
Suggested mechanism in the premenstrual worsening of asthma
fall in progesterone
In severe cases, may be improved by treatment with high doses of progesterone or gonadotropin-releasing factors
124
Mechanism of stress-induced asthma
induce bronchoconstriction through cholinergic reflex pathways
Paradoxically, very severe stress such as bereavement usually does not worsen, and may even improve, asthma symptoms
125
Part of the airway that is predominantly involved in airway inflammation in asthma
Bronchi
Inflammation in the respiratory mucosa from the trachea to terminal bronchioles
126
Physiologic abnormality of asthma
Airway hyperresponsiveness
127
May lead to irreversible narrowing of the airways in asthma
Airway remodelling
Early use of ICS – reduce decline in lung function
128
Prodromal symptoms that may precede an asthma attack (3)
* Itching under the chin
* Discomfort between the scapulae
* Inexplicable fear (impending doom)
129
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)
>12%
200-mL
15 mins
2-4 week
130
Now being used as a non-invasive test to measure eosinophilic airway inflammation
Fractional exhaled NO
Elevated in asthma
Reduced by ICS - may be a test of compliance with therapy
131
The most effective bronchodilator
β2-agonist
132
Adverse effects of β2-agonist (3)
Muscle tremor
Palpitations
Hypokalemia
133
Drugs that prevent cholinergic nerve-induced bronchoconstriction and mucus secretion
Anticholinergic
Less effective than β2-agonist as they inhibit only the cholinergic reflex component of bronchoconstriction
134
Examples of LAMA
tiotropium bromide
| glycopyrronium
135
Example of SAMA
ipratropium bromide
136
Most common side effect of anticholinergic
Dry mouth (esp in elderly)
Other side effects:
Urinary retention
Glaucoma
137
Drugs that inhibits phosphodiesterases in airway smooth-muscle cells
Theophylline
Dose required for bronchodilation commonly cause side effects
May reduce corticosteroid insensitivity in severe asthma
138
A soluble salt of theophylline
IV aminophylline
Via slow IV infusion – in patients with severe exacerbation that are refractory to SABA
139
The most effective controllers for asthma
Inhaled corticosteroids
Reduction in AHR is seen in chronic ICS therapy
140
Local side effects of ICS that may be reduced with the use of a large- volume spacer device (2)
Hoarseness (dysphonia)
| Oral candidiasis
141
Dose of prednisone in asthma
30–45 mg once daily for 5–10 days
142
Block cys-LT1 -receptors and provide modest clinical benefit in asthma
Antileukotrienes (montelukast and zafirlukast)
less effective than ICS in controlling asthma and have less effect on airway inflammation
143
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
Antileukotrienes
144
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
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
Steroid-sparing therapies in asthma (5)
```
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
a blocking antibody that neutralizes circulating IgE without binding to cell-bound IgE and, thus, inhibits IgE-mediated reactions
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
Anti-IL5 drugs (3)
Mepolizumab
Reslizumab
Benralizumab
148
A bronchoscopic treatment using thermal energy to ablate airway smooth muscle in accessible bronchi
Bronchial Thermoplasty
149
In stepwise therapy of asthma, use of a reliever medication more than ____ indicates the need for regular controller therapy
twice a week
150
This finding in asthma is an indication of impending respiratory failure and requires immediate monitoring and therapy
normal or rising PCO2
| PCO2 is usually low due to hyperventilation
151
In treatment of acute severe asthma, a high concentration of oxygen should be given by face mask to achieve oxygen saturation of
>90%
152
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.
Magnesium sulfate
153
There are two major patterns of difficult asthma (2)
- Persistent symptoms and poor lung function, despite appropriate therapy
- Have normal or near normal lung function but intermittent, severe (sometimes life-threatening) exacerbations
154
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
Corticosteroid-Resistant Asthma
155
Asthma subtype that show chaotic variations in lung function despite taking appropriate therapy
Brittle Asthma
156
Asthma subtype that show a persistent pattern of variability and may require OCS or, at times, continuous infusion of β2-agonists
Type 1 brittle asthma
157
Asthma subtype that show generally normal or near-normal lung function but precipitous, unpredictable falls in lung function that may result in death
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
The most effective therapy in type 2 brittle asthma
subcutaneous epinephrine
suggests that the worsening is likely to be a localized airway anaphylactic reaction with edema
159
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
True
160
Approximately ______ of asthmatic patients who are pregnant improve during the course of a pregnancy, ______ deteriorate, and _________ are unchanged
one-third
161
Better OCS to be used in asthma in pregnancy
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
Some patients report a temporary worsening of asthma when they first stop smoking, possibly due to the
loss of the bronchodilating effect of NO in cigarette smoke
163
Asthmatic patients with FEV1 ____ of their normal levels should also be given a boost of OCS prior to surgery.
<80%
164
On of the aims of asthma therapy is the peak expiratory flow circadian variation of
<20%
165
# Define controlled asthma based on:
```
Daytime symptoms
Limitation of activities
Nocturnal symptoms/awakening
Need for reliever/rescue treatment
Lung function (PEF or FEV1)
```
```
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
# Define partly-controlled asthma based on:
```
Daytime symptoms
Limitation of activities
Nocturnal symptoms/awakening
Need for reliever/rescue treatment
Lung function (PEF or FEV1)
```
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
Define uncontrolled asthma
3 or more features of partly controlled asthma
168
Pulmonary hypertension is defined as an elevation in pulmonary arterial pressures (mean pulmonary artery pressure [PAP] _____ or an estimated systolic PAP________)
>22 mmHg
| >36 mmHg
169
The most common cause of death in pulmonary arterial hypertension
Decompensated right heart failure
170
More common symptoms of PH (2)
dyspnea and/or fatigue
Less common symptoms: edema, chest pain, presyncope, and syncope
171
The most important initial screening test of pulmonary hypertension
Echocardiogram with bubble study
172
The gold standard for diagnosis and assessment of disease severity
Invasive hemodynamic monitoring
173
In patients suspected with PH with normal echocardiogram but with unexplained dyspnea or hypoxemia, it is reasonable to proceed to
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
Isolated reduction in diffusing capacity of the lungs for carbon monoxide (DLCO) in pulmonary function test is a classing finding in
Pulmonary arterial hypertension
175
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
6-minute walk test
176
T or F. Since-breathing disorders is an important cause of mild PH, sleep study must be done to patients suspected to have PH
False. Sleep study is generally necessary only when indicated by the patient’s history
177
Remains the gold standard both to establish the diagnosis of PH and to guide selection of appropriate medical therapy
RHC with pulmonary vasodilator testing
178
The definition of precapillary PH or PAH requires (3):
* 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
Passive post capillary PH is defined as (2)
* PCWP ≥15 mmHg
| * Transpulmonary gradient <12 mmHg
180
Reactive post capillary PH is defined as (3)
* PCWP ≥15 mmHg
* Transpulmonary gradient >12 mmHg
* Incresed PVR
181
Preferred for vasodilator testing in right heart catheterization
Vasodilators with a short duration of action (i.e. inhaled nitric oxide (NO), or inhaled epoprostenol)
182
Positive response for vasodilator testing during RHC
a decrease in mPAP by ≥10 mmHg to an absolute level ≤40 mmHg without a decrease in CO
183
Treatment that may be given to PH patents with positive response to RHC with pulmonary vasodilator testing
long-term treatment with calcium channel blockers (CCB)
184
WHO Group I PH
Pulmonary arterial hypertension – rare cause
185
PAH is defined as a ________ in resting mean pulmonary arterial pressure (mPAP) ________ , PVR________, and PCWP or LVEDP of _________based on a RHC
sustained elevation
≥25 mmHg
> 240 dyne-s/cm5
≤15 mmHg
186
Rare infectious cause of PAH
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
Only connective tissue diseases associated with PAH
Systemic sclerosis
Patients who eventually develop scleroderma-associated PAH tend to be older at the time of scleroderma diagnosis
188
Systemic sclerosis subtype that is most commonly associated with PAH
Cutaneous scleroderma
189
WHO Group II PH
Pulmonary hypertension associated with left heart disease
190
Which form of HF that has higher overall risk of PH
HFpEF
191
T or F. PH portends a poor prognosis in all forms of HF
True
192
Hall mark of WHO Group II PH
Elevated left atrial pressure with resulting pulmonary venous hypertension
193
WHO Group III PH
Pulmonary hypertension associated with lung disease
194
the second most common cause of PH
Intrinsic lung disease
195
The most studied form of interstitial lung disease associated with PH
Idiopathic pulmonary fibrosis
196
WHO Group IV PH
PH with chronic thromboembolic disease
197
Important and often the dominant factor in WHO Group IV PH
Obstruction of the proximal pulmonary vasculature
198
Infectious cause of PH which is one of the most common cause globally
Schistosomiasis
Occurs in the setting of hepatosplenic disease and portal hypertension
199
T or F. Without treatment PAH is invariably fatal
True
200
Drugs that addresses the imbalance of arachidonic acid metabolites with reduced prostacyclin levels and increased thromboxane A2 production in PAH
Prostanoids
201
The first prostanoid available for the management of PAH
Epoprostenol
* Continuous intravenous infusion
* Improves functional capacity and survival in PAH
202
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
Phosphodiesterase-5 (PDE5) inhibitors (e.g., sildenafil)
203
An oral nonprostanoid diphenylpyrazine derivative used in the treatment of PAH that binds the prostaglandin I2 (IP) receptor with high affinity
Selexipag
204
Non-selective ET-1 receptor antagonists that improves hemodynamics and exercise capacity and delays clinical worsening of PAH
Bosentan
205
A selective ET-A receptor antagonist used in treatment of PH
Ambrisentan
206
Drug used in PH that prolong the vasodilatory effect of NO, especially within the pulmonary arterial bed where high concentrations of cGMP are found
cGMP phosphodiesterase type 5 (PDE5) inhibitors
207
Two PDE5 inhibitors used for the treatment of PAH:
* Sildenafil
| * Tadalafil
208
A clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure
ARDS
209
2 most common cause of ARDS
Pneumonia and sepsis
Other causes:
1. Aspiration of gastric contents
2. Trauma
3. Multiple transfusion
4. Drug overdose
210
Most common trauma injury that causes ARDS (3)
1. Pulmonary contusion
2. Multiple bone fractures
3. Chest wall trauma / flail chest
Head trauma, near-drowning, toxic inhalation, and burns – rare causes
211
Clinical variables associated with the development of ARDS (5)
1. Older age
2. Chronic alcohol abuse
3. Metabolic acidosis
4. Pancreatitis
5. Severity of critical illness
212
Trauma patients with APACHE II score of ___ have 2.5-fold increased risk for ARDS
≥ 16
213
3 phases of ARDS
1. Exudative phase
2. Proliferative phase
3. Fibrotic phase
214
Phase of ARDS wherein edema fluid that is rich in protein accumulates in the interstitial and alveolar spaces
Exudative phase
215
Phase of ARDS with neutrophil as the predominant cells
Exudative phase
216
Phase of ARDS wherein condensed plasma proteins aggregate in the air spaces with cellular debris and dysfunctional pulmonary surfactant to form hyaline membrane whorls
Exudative phase
217
Prominent in early ARDS: hypocapnia or hypercapnia
Hypercapnia
218
Exudative phase of ARDS occur in the _____ days of illness
1st 7 days
219
ARDS patient experience onset of respiratory symptoms usually within ____ after initial insult
12-36 hours
220
12-36 hours
¾
221
Proliferative phase of ARDS occur in the day _____ of illness
Day 7 to day 21
Most patients recover rapidly and are liberated from mechanical ventilation
222
Phase of ARDS wherein some patients develop progressive lung injury and early changes of pulmonary fibrosis
Proliferative phase
223
Histologically, 1st signs of resolution are seen in this phase of ARDS
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
Phase of ARDS with lymphocyte as its predominant cell
Proliferative phase
225
T or F. All patient with ARDS enter the 3rd phase
False. Some patients enter fibrotic phase that may require long-term support on mechanical ventilators and/or supplemental oxygen
226
Phase of ARDS characterized by arked disruption of acinar architecture resulting to emphysema-like changes with large bullae
Fibrotic
227
2 principal mechanism of ventilator-induced lung injury:
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
Clinicians must empirically measure the “best PEEP” at the bed side to determine the optimal settings that best promotes (3)
1. alveolar recruitment
2. minimizes alveolar overdistention and hemodynamic instability
3. Provides adequate Pao2 while minimizing Fio2
229
This position may improve arterial oxygenation in ARDS
Prone positioning
230
Strategy in mechanical ventilation that transiently increase PEEP to high levels to “recruit” atelectatic lung can increase oxygenation
Recruitment maneuvers
231
Rescue therapy for ARDS that improve mortality
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
T or F. Fluid restriction therapy and diuretics are important aspects in ARDS management
True
233
This drugs may be given to improve the patient-ventilator synchrony in ARDS
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
T or F. Glucocorticoid is routinely given in severe ARDS
False.
235
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:
* 34.9% for mild ARDS
* 40.3% for moderate ARDS
* 46.1% with severe ARDS
236
Mortality in ARDS is attributable to (2)
1. Sepsis
| 2. Nonpulmonary organ failure
237
Major risk factors for ARDS mortality (4)
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
In ARDS, patients usually recover maximal lung function within
6 months
239
Recovery of lung function post ARDS is strongly associated with the _________
extent of lung injury in early ARDS
240
Direct lung injury that causes ARDS (5)
1. Pneumonia
2. Aspiration of gastric contents
3. Pulmonary contusion
4. Near-drowning
5. Toxic inhalation injury
241
Indirect lung injury that causes ARDS (6)
1. Sepsis
2. Severe trauma
3. Multiple transfusions
4. Drug overdose
5. Pancreatitis
6. Postcardiopulmonary bypass
242
Mild, moderate and severe ARDS are defined as
Mild: Pao2/Fio2 200 mmHg - 300 mmHg
Moderate: Pao2/Fio2100 mmHg - 200 mmHg
Severe: Pao2/Fio2 ≤ 100 mmHg
243
Class A recommendation for management of ARDS
Low tidal volume
244
Class B recommendations for management of ARDS (5)
1. Minimized left atrial filling pressures
2. High-PEEP or “open lung”
3. Prone position
4. ECMO
5. Early neuromuscular blockade
245
```
Goals and limits in ARDS based on:
Tidal volume
Plateau pressure
RR
FiO2
SpO2
pH
MAP
```
```
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
Most common way for microorganism to gain access to the lower respiratory tract
Aspiration from the oropharynx
247
Mechanical host defense that traps microbes on the airway lining
Branching architecture of the tracheobronchial tree
248
Extremely efficient at clearing and killing pathogens in the respiratory tract
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
The two most likely sources of an altered alveolar microbiota
1. Viral upper respiratory tract infections for CAP
| 2. Antibiotic therapy for HAP/VAP
250
Phase of pneumonia characterized by presence of a proteinaceous exudate—and often of bacteria—in the alveoli
Edema
1st phase
Rarely evident in clinical or autopsy specimens
251
Phase of pneumonia characterized by presence of erythrocytes in the cellular intra-alveolar exudate
Red hepatization
252
Phase of pneumonia characterized by neutrophil influx
Red hepatization
Bacteria are occasionally seen in pathologic specimens
253
Phase of pneumonia characterized by lysis and degradation of the erythrocytes and no new erythrocytes are extravasating
Gray hepatisation
254
Phase of pneumonia characterized by abundance of fibrin deposition
Gray hepatization
255
Predominant cell in gray hepatization
Neutrophil
256
Phase of pneumonia characterized by disappearance of bacteria and successful containment of the infection and improvement in gas exchange
Gray hepatization
257
Predominant cell in resolution phase of pneumonia
macrophage
258
Phase of pneumonia characterized by clearance of the debris of neutrophils, bacteria, and fibrin
Resolution
259
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
Resolution
260
Most common pattern in nosocomial pneumonia
Bronchopneumonia pattern
Because of the microaspiration mechanism
261
Most common pattern in bacterial CAP
Lobar pattern
262
Most common cause of CAP
Streptococcus pneumoniae
263
Atypical bacteria causing pneumonia (3)
1. Mycoplasma pneumonia
2. Chlamydia pneumonia
3. Legionella
264
Most common viruses causing CAP (3)
1. Influenza
2. Parainfluenza
3. Respiratory syncytial viruses
265
May cause necrotizing pneumonia (2)
S. aureus pneumonia
P. aeruginosa
Complicate influenza infection
266
Risk factors for CAP (5)
1. Alcoholism
2. Asthma
3. Immunosuppression
4. Institutionalization
5. Age of ≥70 years
267
Risk factors for pneumococcal pneumonia (8)
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
Risk factors for CA-MRSA pneumonia
Skin colonization or infection with CA-MRSA
269
Risk factors for Enterobacteriaceae-casued pneumonia (5)
1. Recently been hospitalized
2. Received antibiotic therapy
3. Alcoholism
4. Heart failure
5. Renal failure
270
Risk factors for P. aeruginosa pneumonia
Severe structural lung disease (bronchiectasis, cystic fibrosis, or severe COPD)
271
Risk factors for Legionella pneumonia (8)
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
Gross hemoptysis is suggestive of what pneumonia
CA-MRSA pneumonia
273
Chest radiography finding of pneumatoceles is suggestive of what cause of pneumonia
S. aureus
274
To be adequate for culture, a sputum sample must have ___ neutrophils and ____ squamous epithelial cells per low-power field
>25
| <10
275
Main purpose of sputum GS
ensure that a sample is suitable for culture
276
T or F. Blood cultures must be done in all patients with CAP
False.
Certain high risk patients must have blood cultures:
1. Neutropenia
2. Asplenia
3. Complement deficiencies
4. Chronic liver disease
5. Severe CAP
277
Urinary antigen tests detects what antigen that may be causative of pneumonia (2)
Pneumococcal
Legionella (serogroup 1)
Both tests can detect antigen even after the initiation of appropriate antibiotic therapy
278
Accounts for most community-acquired cases of Legionnaires’ disease
Legionella pneumophila serogroup 1
279
A 20-variable prognostic model used to identify patients at low risk of dying
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
Mortality rates of the 5 classes of Pneumonia Severity Index (PSI)
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
A 5-variable severity-of-illness scoring for pneumonia
CURB-65 criteria
282
5 variables of CURB-65 criteria
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
CURB-65 score that can be treated outside the hospital
Score 0
30-day mortality rate is 1.5%
284
CURB-65 score indicating that patient should be hospitalized unless the score is entirely or in part attributable to an age of ≥65 years
Score of 1 or 2
285
CURB-65 score may require ICU admission
≥ 3
286
Mortality rate of CURB-65 score of ≥3
22%
287
Minimal inhibitory concentration (MIC) cutoffs for penicillin for susceptible, intermediate, and resistant
* ≤2 μg/mL for susceptible
* >2–4 μg/mL for intermediate
* ≥8 μg/mL for resistant
288
Isolates resistant to drugs from ____ antimicrobial classes with different mechanisms of action are considered MDR strains
three or more
289
The most important risk factor for antibiotic-resistant pneumococcal infection is
use of a specific antibiotic within the previous 3 months
290
Most important distinction of CA-MRSA from the hospital-acquired MRSA
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
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
Ceftaroline
292
Pneumonia patients slow to respond to therapy should be reevaluated at about
day 3
sooner if their condition is worsening rather than simply not improving
293
Indication for complete drainage by chest tube of pleural effusion (4)
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
Chest radiographic abnormalities of pneumonia may resolve at how many weeks?
4-12 weeks
295
Outpatient mortality rate of pneumonia
<5%
296
Inpatient mortality rate of pneumonia
2 to 40%
297
Non-MDR pathogens predominate if VAP develops in the first ____ of the hospital stay
5–7 days
298
The most obvious risk factor for VAP
ET tube
May prevent large-volume aspiration, but microaspiration is exacerbated by secretions pooling above the cuff
299
Diagnostic threshold of ETA sample for VAP
10^6 cfu/mL
300
Diagnostic threshold of protected specimen brush method for VAP
10^3 cfu/mL
301
Achilles heel of Quantitative-Culture Approach of diagnosing VAP
The effect of antibiotic therapy
With sensitive microorganisms, a single antibiotic dose can reduce colony counts below the diagnostic threshold
302
The major risk factor for infection with MRSA and extended-spectrum β-lactamase–positive strains
Frequent use of β-lactam drugs, especially cephalosporins
303
Etiologic agents of VAP that are intrinsically resistant to many of the empirical antibiotic regimens employed (3)
1. Acinetobacter species
2. Stenotrophomonas maltophilia
3. Burkholderia cepacia
304
There is lower incidence of atypical pathogens in VAP except for
Legionella
305
Major complication of VAP
Prolongation of mechanical ventilation
306
Mortality rate of VAP
50–70%
307
Pneumonia caused by this pathogen is simply a marker for a patient whose immune system is so compromised that death is almost inevitable
S. maltophilia
308
Risk factors for pneumonia caused by MDR gram-negative bacteria and MRSA (7)
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
Risk factors for pneumonia caused by nosocomial MRSA (6)
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
Risk factors for pneumonia caused by CA-MRSA (7)
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
Possible cause of CAP when there is history of exposure to bats
H. capsulatum
312
Possible cause of CAP when there is history of exposure to birds (2)
1. H. capsulatum
| 2. Chlamydia psittaci
313
Possible cause of CAP when there is history of exposure to rabbits
Francisella tularensis
314
Possible cause of CAP when there is history of exposure to sheep, goats, parturient cats
Coxiella burnetii
