RC Respirology Flashcards

(1222 cards)

1
Q

What is an abnormal pulsus paradoxus?

A

> /10 mmHg change of systolic BP between inspiration and expiration

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2
Q

DDX for abnormal pulsus

A

Tamponade
Asthma exacerbation
COPD exacerbation
Constrictive pericarditis
PE
Morbid obesity

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3
Q

Effects of hyperoxia on respiratory system

A

Hypercapnia, CO2 retention
Direct O2 toxicity from ROS - interstitial and alveolar edema due to leaky capillary endothelium, hyperoxic bronchitis
Absorption atelectasis
Instability of units with low V/Q ratios causing shunt
Retinopathy of prematurity (not respiratory)

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4
Q

Benefits of HFNC in patients with respiratory failure

A

Heated and humidified - reduces WOB, allows secretion clearance
Provides PEEP - decreases WOB, prevents atelectasis
Provides PEEP - prevents atelectrauma
High flows - washours out upper airway dead space, reliable FiO2 delivery due to minimal entrainment, decreases upper airway resistance

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5
Q

Who should have extubation to HFNC

A

Extubation of surgical patients
Extubation of non surgical patients at low/mod risk of extubation failure

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6
Q

Sources of physiological shunt

A

Bronchial arteries emptying into pulmonary veins
Thebesian veins emptying into left ventricle
Functional shunt: V/Q <1

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7
Q

Limitations/assumptions of the shunt equation

A

CcO2 = CAO2 = perfect diffusion between alveoli and capillaries
We assume PcO2 = PAO2 (from alveolar gas equation)
We assume that SaO2 = 1
Assumes all gas exchange occurs with ideal V/Q matching.

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8
Q

Differences between central and mixed venous gas

A

ScvO2 = central line, normal is 65-70% (>80% (high PaO2 or left to right shunt) vs <65% (impaired tissue oxygenation))
SvO2 = pulmonary artery, normal is 60-65%

basically ScvO2 should have higher O2 because it doesn’t get the low O2 blood from the IVC

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9
Q

DDX for high O2 Extraction Ratio

A

Sepsis, fever
Shock
Seizures
Hyperthyroidism
Hypoxemia
Anemia

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10
Q

DDX for low O2 Extraction Ratio

A

Hypothyroidism
Hypothermia
Sedation
Mitochondrial dysfunction in sepsis
Cyanide toxicity
Hyperbaric oxygen
Hyperoxia
Polycythemia

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11
Q

Impact of Positive Pressure Ventilation on the heart

A

Decreased preload to RV and LV
Increased afterload to RV, decreased afterload to LV
Overall, decreased SV and CO, decreased cardiac work

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12
Q

Impact of Positive Pressure Ventilation on dead space

A

Increased zone 1 respiration with high V/Q areas

Increases both alveolar and anatomic dead spaces
Lung volume is raised resulting in radial traciton on the airways increasing volume of anatomic dead space
Raised airway pressures divert blood flow away from ventialated regions causing high v/q ratio or even unperfused areas
Most common in uppermost regions of the lung.
Capillaries pressures fall below airway pressure and they collapse

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13
Q

Different Ventilator modes and settings

A

Assisted= mandatory patient triggered
Controlled= mandatory Time/volume triggered
Supported= spontaneous (patient triggered) flow terminated
PCV- you set inspiratory pressure. Volume will vary
VCV - you set TV peak flor and flow pattern. Pressure will vary
PSV - (Spontaneous Pressure Support Ventilation) al breaths supported (whatever TV the patient generates)
ASV - set EPAP, PS mirrors ventilation (higher at low flow periods)
SIMV (synchronized Intermittent Mandatory Ventilation- set RR with either Volume or PRessure target), patient can do what they want in between the set breaths
APRV - airway pressure release ventilation - Bilevel ventilation where you set PEEP and plateau. rescue therapy for ARDS, helps with recruitment to help with oxygenation, spontaneous breathing (increased WOB), risk of volutrauma, risk of DH

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14
Q

What are PIP, Pplat, driving pressures, delta P, airway resistance

A

PIP: (peak inspiratory Pressure) P to overcome resistance (airways, ETT) and lung elastic properties, target <35
Pplat: P to distend alveoli, reflects compliance, target <30 cmH2O
Driving pressure: Pplat - PEEP
Delta P: PIP-Pplat, reflects resistance: both elevated within 5 means reduced lung compliance or chestwall/diaphragm/pleural. Only Elevated PIP means increased airway resistance
Airway resistance: PIP-Pplat/Flow

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15
Q

Types of Respiratory Maneuvers on the ventilator

A

Inspiratory hold → Pplat
Expiratory hold → intrinsic PEEP
Only in volume control

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16
Q

DDx of reduced peak inspiratory pressure

A

Air leak
Hyperventilation

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17
Q

What do changes to the volume pressure curve represent on a ventilator?

A

Slope = static compliance
Width = dynamic compliance and airway resistance
Bird beaking = over distension = turn TV down

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18
Q

What are Static and dynamic compliance on a ventilator?

A

Static: chest wall and lung tissue compliance
Dynamic: chest wall, lung tissue compliance and airway resistance

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19
Q

what is the DDX for sudden increase in mechanical ventilation in critically ill patients

A

Increased dead space - collapsed lung, mucous plug, mainstem intubation/dislodged
Increased demand - sepsis, fever
Pain, anxiety
Decreased compliance

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20
Q

Benefits of PEEP

A

Improve oxygenation -improve atelectasis/VQ, moves peripheral edema into interstitium
Lessens required FIO2 and O2 toxicity
Improves lung compliance - think of equation Compliance = delta V/Delta P
Prevent atelectrauma
Decrease WOB
Decrease LV work/afterload

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21
Q

Mechanisms of hypotension with PEEP

A

Reduced preload to RV and LV
Increased RV afterload, RV failure
Reduced LV compliance

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22
Q

Consequences of autoPEEP

A

Barotrauma
Dynamic hyperinflation
Decreased lung compliance
Decreased tidal volumes and minute ventilation
Increased WOB
Cardiac - decreased preload, decreased CO, increased PVR
Neuro - increased ICP due to reduced central venous return

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23
Q

DDX of increased autoPEEP

A

Increased airway resistance e.g. bronchospasm, kinked tube, clogged tube
Increased tidal volume
Increased respiratory rate
Increased I:E time or ratio
Decreased expiratory time
Increased inspiratory time
Decreased inspiratory flow rate

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24
Q

Treatment of autoPEEP

A

Treat bronchospasm or reason for resistance
Decrease respiratory rate
Decrease tidal volume
Decrease I:E ratio
Increase expiratory time
Increase inspiratory flow rate
Increase or add PEEP **
Permissive hypercapnia ** (reduce demand)
Sedation and paralysis if dyssynchronous, treat anxiety/pain ** (reduce demand)

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25
Relative Contraindications to PEEP
High ICP Hypotensive RV failure Right to left shunt Barotrauma Bronchopleural fistula
26
Causes for difference between PaCO2 and PETCO2
PETCO usually lower Due to anatomical dead space
27
Causes of increased PETCO2
ROSC (increase by 10-20) Effective CPR Hyperthyroidism Hyperthermia Fever, sepsis Hypoventilation Bronchial intubation
28
Causes of decreased PETCO2
Hypotension, shock Cardiac arrest Hypothyroidism Hypothermia Hyperventilation Apnea Extubation, sudden kink
29
Ventilatory parameters for obstructive lung disease
Mode:volume (but no data > pressure) FiO2: SpO2 88-92 PEEP: minimal, 5 RR: 10-12% Vt: <8 mL/kg PBW I:E target: 1:5 Permissive hypercapnia (pH >7.2, pCO2 <90)
30
Ventilatory parameters for ARDS
Mode: volume FiO2: 88-95% PEEP: Modest RR: 25-35 Vt: 4-6 mL/kg/PBW I:E target: 1:2 Permissive hypercapnia (pH >7.2) Pplat
31
Physiological benefits of permissive hypercapnia
Reduced autoPEEP Reduce barotrauma Decrease WOB
32
Rationale for permissive hypercapnia in ventilation
Obstruction - prevent autoPEEP Restriction - low tidal volumes
33
Possible complications of permissive hypercapnia
Increased ICP Decrease seizure threshold Arrhythmias, irritable myocardium Increased PVR 2/2 acidosis Decreased placental flow
34
In addition to ventilator settings, what else do you have to take into consider in Mechanical Ventilation asthma?
Not opioids for sedation 2/2 histamine Large ETT to reduce resistance Consider inhaled isoflurane Consider heliox Consider Hodder’s maneuver Consider ECMO
35
Characteristics of Heliox
Low density Density is important in turbulent flow (large airways) Viscosity is important in laminar flow (smaller airways)
36
Importance of the Winters Equation
Tells you what CO2 should be if appropriately compensated Use this to determine goal Ve
37
Berlin's criteria for ARDS - NOTE NEW CRITERIA!
Within 7 days of a known insult or worsening symptoms Non cardiogenic pulmonary edema, not due to intravasc volume overload Bilateral pulmonary opacities not explained by nodules, atelectasis, effusion, etc. (CXR OR CT, or lung ultrasound by trained professional) Seen in 2 quadrants (bilat or unilat) Severity grading on PEEP 5 PaO2/FiO2<300 SpO2/FiO2 <315
38
Causes of ARDS
Inhalation exposures Aspiration Fresh water, salt water aspiration, drowning Fat embolism Reperfusion injury Infections, pneumonia, sepsis Pancreatitis Transfusion reaction
39
Pathology of ARDS
1. Early exudative: 1 week, high permeability pulmonary edema, proteinaceous fluid fills alveoli, hyaline membrane formation, pathology shows DAD 2. Fibroproliferative: 2 weeks, interstitial inflammation, disordered healing, fibrosis 3. Fibrotic: fibrosis, obliteration of normal lung architecture
40
Image findings of ARDS
Dependent opacities, consolidation Bilateral, symmetrical
41
Ways to improve oxygenation in ARDS
Increase PEEP, mortality benefit in mod-severe Prone positioning, 12hrs/day, PF <150 mortality benefit (It should be administered within 48 hours, evaluated daily and stopped within 48 hrs if possible) Euvolemia Steroids in some Neuromuscular blockade Inhaled NO ECMO
42
Physiological benefits of prone positioning in ARDS
Improve V/Q matching Improve secretion mobilization + drainage Decrease compressive effects of heart
43
Indications for ECMO
PaCO2 >60 for >6 hours PF <80 for >6 hours PF <50 for >3 hours Mechanically ventilated <7 days, BMI <40, age 18-65
44
Contraindications to ECMO
Disseminated malignancy Known severe brain injury Severe chronic organ dysfunction Severe pulmonary hypertension
45
Complications of Positive Pressure Ventilation
Hypotension Barotrauma VALI VAP Airway complications e.g. stenosis, tracheobronchomalacia, fistula formation Critical illness polyneuropathy, myopathy
46
Risk factors for barotrauma
High Pplat* High PIP* High PEEP* Low compliance* e.g. ILD, COPD, overload
47
Maneuvers to reduce risk of barotrauma
Reduce RR Reduce Vt Increase expiratory time Permissive hypercapnia Increase sedation Reduce PEEP
48
Benefits of tracheostomy
Reduced sedation Phonation Better secretion management, better mouth care Allows mobility Prevents laryngeal injury Can leave ICU
49
Acute complications of tracheostomy
Bleeding Surgical site infection Dislodgement Tube is kinged or clogged Laryngeal nerve damage Pneumothorax
50
Chronic complications of tracheostomy
Dislodgement Trach blockage Tracheal stenosis Tracheobronchomalacia Tracheoesophageal fistula Tracheoarterial fistula
51
What is VALI?
Due to volutrauma Alveolar overdistension Presents with edema, hemorrhage, loss of compliance
52
Indicators of readiness to wean
Underlying resp condition resolved or improving/on active treatment GCS >8 PaO2 >60 on FiO2 requirements <40% on PEEP <8 PF ratio >150 PaCO2 normal Adequate cough Not requiring frequent suctioning e.g.
53
Abnormal RSBI (Rapid Shallow Breathing Index)
RR/TV >105 Predictive of failed extubation
54
Predictors of successful weaning during SBT
RR/VT = RSBI <105 Maintaining adequate ventilation Maintaining adequate oxygenation No signs of severe fatigue
55
Definition of extubation failure
Reintubation within hours-days
56
Risk factors for extubation failure
Age >65 Underlying cardiorespiratory disease RSBI >105 Abundant endotracheal secretions Weak or absent cough Positive fluid balance in last 24 hours Respiratory failure was for cardiac origin, PNA, neurological condition
57
Factors that may limit weaning
Reduced drive from over sedation or neurological problem Underlying disease not yet resolved Respiratory muscle weakness, deconditioning Development of atelectasis, mucous plugging - poor/weak cough VAP/VALI development Oversedation Under Sedation - anxiety, pain Neuropathy or myopathy from prolonged intubation Malnutrition - respiratory muscle weakness Overnutrition - increased CO2 production Cardiomyopathy, cardiac ischemia Anemia
58
Clinical signs of failure during SBT
Anxiety, agitation, diaphoresis Hypertension or hypotension - not between 90-180 Tachycardia - HR >140, arrhythmia Tachypnea - RR >35 x 5 mins Increased work of breathing - accessory muscle use, thoracoabdominal paradox Fall in O2 (<90%), increase in CO2 - hypoxemia and hypercapnia Stridor
59
What causes Right shift in the hb-dissociation curve
Increased CO2 (Bohr effect) Increased H Increased temperature Increased 2,3 DPG
60
What causes Left shift in the hb- dissociation curve
Decreased CO2 (Bohr effect) Decreased H Decreased temperature Decreased 2,3 DPG Increased CO
61
Determinant of PaO2
PAO2 - POI2, PaCO2 Architecture of the lungs
62
Major determinants of SaO2
PaO2 Temperature H CO2 2,3 DPG
63
DDX for saturation gap
Carboxyhemoglobinemia Methemoglobinemia Sulfhemoglobinemia
64
DDX for lower SpO2 for given PaO2
Nail polish Pigments, methylene blue Poor circulation - Raynaud’s, peripheral vascular disease, shock Hemoglobinemia - e.g. methemoglobinemia, sulfhemoglobinemia, thalassemia, sickle cell anemia, spherocytes etc Motion or artifact Technical factors
65
Clinical manifestations of CO poisoning
Headaches, decreased LOC, personality changes, headaches, seizures Arrhythmias, cardiac ischemia Cherry red skin and lips
66
Treatment options for CO poisoning
Supplemental oxygen Hyperbaric oxygen Eucapnic hyperventilation
67
Indications for hyperbaric oxygen in CO poisoning
Severe end organ sx e.g. MI CO-Hb >/25% CO-Hb >/15% if pregnant Severe metabolic acidosis pH <7.1
68
Blood gas findings in CO poisoning
PaO2 normal SpO2 normal SaO2 decreased CaO2 decreased CvO2 decreased
69
Blood gas findings in cyanide poisoning
PaO2 normal SpO2 normal SaO2 decreased (I think Normal) CaO2 normal CvO2 increased
70
Treatment for cyanide poisoning
Supplemental oxygen Hydroxocobalamin Nitrites Avoid dialysis
71
Safe amount of lidocaine to prevent toxicity
5 mg/kg without epi 7 mg/kg with epi
72
Treatment of lidocaine toxicity
BZD Lipid emulsion
73
At what pressure is O2 delivered at in hyperbaric O2?
2.5-3 atm
74
Contraindications to HyperBaric Oxygen Therapy
Pneumothorax untreated - absolute Obstructive lung disease - relative Blebs or bullous disease - relative
75
Indications for HyperBaric Oxygen Therapy
CO poisoning Venous or arterial air embolism Decompression sickness
76
Medications that can cause methemoglobinemia
Lidocaine, benzocaine Methylene blue Metoclopramide Dapsone Nitrates Primaquine
77
Indications for methylene blue for methemoglobinemia
Levels >30% Very symptomatic
78
Indications for intubation in someone with thermal/fire airway injury
Neck, facial burns Laryngeal injury - Stridor Tracheobronchial injury - cough, wheezing, melanoptysis Paryncheal injury Systemic toxicity e.g. CO poisoning etc
79
Broad categories for International Classification of Sleep Disorders
Insomnia Sleep disordered breathing - OSA, CSA, OHS, Nocturnal Desaturation Hypersomnolence Parasomnias Sleep related movement disorders Circadian rhythm sleep wake disorders Other
80
Definition of compliance with Sleep Therapy
4 hrs per night At least 70% of nights in last month
81
As per CMA guide, which patients with OSA should not be driving?
Moderate-severe OSA, not compliant Compliant but involved in MVC where they were at fault - x 1 month until compliance reassessed Drivers admit to experiencing excessive sleepiness during major wake periods or while driving
82
As per the Ontario MTO, who should not be driving?
AHI >/30 in treated or untreated
83
As per CMA guide, which patients with narcolepsy should not be driving?
Uncontrolled cataplexy (on or off treatment) in the past 12 months Uncontrolled daytime sleep attacks or sleep paralysis in the past 12 months Generally no long distance commercial driving
84
For a commercial driver with OSA, what conditions need to be met for them to drive?
AHI <20 On effective treatment Does not experience excess sleepiness during major wake periods
85
Which drivers do we screen for OSA?
Everyone should be screened with questionnaires, BMI and studies as needed Recertified annually
86
When can commercial drivers be recertified?
PAP - one week, good compliance, good AHI, no sleepiness Oropharyngeal surgery or trach - one month, good AHI, no sleepiness Bariatric surgery - six months, good AHI, no sleepiness
87
Distribution of sleep
N1 - 5% N2 - 50% N3 - 20% REM - 25%
88
Sleep spindle
Usually in N2 Fast burst 0.5-2s of 12-15 Hz activity
89
K complex
Usually in N2 Go up first, then down High-Amplitude/Biphasic
90
How much theta waves do you require in N1/N2 sleep?
At least 50% of the epoch
91
How much delta do you need in N3 sleep?
At least 20% of the time
92
Other names for N3 sleep
Slow wave sleep Deep sleep
93
Features of REM sleep
Low amplitude, mixed frequency REM atonia → low chin EMG Rapid eye movements May see sawtooth waves
94
How do sleep disorders change during REM sleep
OSA worsens, CSA improves (reduced chemosensitivity so won't be as sensitive to changes in Co2 Hypovent and hypoxemia in NMD or chest wall disorders (bc loss of accessory muscles during atonia) **
95
What does a short REM latency suggest? What are the causes of REM rebound?
1. Narcolepsy 2. REM Rebound 2a. Depression 2b. Medication withdrawal e.g. SSRIs, BZD, alcohol 2c. REM sleep deprivation 2d. Patients undergoing CPAP titration
96
Causes of REM suppression
SSRIs Monoamine oxidase inhibitors Sedative hypnotic drugs, barbiturates Antiepileptics Alcohol
97
Medications stimulate breathing vs suppress breathing
Stimulate: theophylline, acetazolamide, progesterone, thyroid hormone Inhibit: BZD, barbiturates, gabapentinoids, alcohol
98
Effect of aging on sleep
Decrease in N3 Increase in N1 and N2 No change in REM Increased WASO - wake after sleep onset More arousal Lower sleep efficiency Body’s clock shifts earlier
99
Physiological changes during sleep
Decreased BP, HR, CO (increase in phasic REM) Decreased RR, VT, VE; RR generally increase in REM PaCO2 increase 3-5 mmHg PaO2 decrease 5-8 mmHg; SpO2 decrease 1-2% Increased upper airway resistance
100
Minimum requirements for an adequate sleep study
At least 2 hours of sleep Other normal values (not required): 80% efficiency, <30 mins sleep onset, <90 mins REM onset
101
Components of a PSG
EEG EOG EMG ECG Airflow (2) Respiratory efforts (2) SpO2 CO2 measurement
102
Ways to measure airflow
Oronasal thermistor - apnea Nasal pressure transducer - hypopnea, RERA
103
Ways to measure respiratory effort measured
RIP belt (respiratory inductance plethysmography) Esophageal pressure monitoring Diaphragmatic EMG
104
When should patients with sleep apnea be followed up on?
Within 4 weeks if high risk Within 6 months for all others
105
Who is a level II-IV sleep study appropriate for? What are Contraindications?
Moderate-high pretest probability Do not suspect other sleep disorders Do not have other comorbid diseases Not a titration study
106
Criteria for moderate-high pretest probability of OSA
Excessive Daytime Sleepiness on most days with 2 of the following: Snoring Witnessed apneic episodes Witnessed choking during sleep Witnessed gasping during sleep Diagnosed HTN
107
Criteria for comorbid/complicated disease (sleep disordered breathing)
Cardiorespiratory disease History of stroke Respiratory muscle weakness, NMD Suspicion for hypoventilation
108
Levels of Home Sleep Apnea Testing
II: Full PSG but done at home III: airflow, effort, ECG, pulse oximetry IV: pulse oximetry
109
Requirements that need to be met to be able to do split night study
Moderate-severe OSA based on at least 2 hours of recordings 3 hours available for titration
110
Definition of apnea vs hypopnea
Apnea: decrease in flow >/90% from baseline x >/10 seconds Hypopnea: decrease in flow >/30% from baseline x >/10 seconds and accompanied by desaturation of SaO2 by 3% or arousal
111
Definition of obstructive vs central HYPOPNEAs
Obstructive: snoring, thoracoabdominal paradox, increased insp flattening of nasal pressure compared to baseline Central: None of the above
112
Definition of mixed apneas
Starts out as central, then obstructive
113
Definition of a RERA
Increase in resp effort or flattening of nasal pressure waveform Event causes arousal or desaturation without meeting appropriate criteria x 10 s
114
Definition of hypoventilation on a PSG
Increase in PaCO2 >55 mmHg x 10 mins Increase in PaCO2 by >/10 mmHg to a value above 50 mmHg x 10 mins
115
AHI vs RDI
AHI = Apnea + hypopnea/total sleep time RDI = Apnea + hypopnea + RERA/total sleep time
116
DDX for EDS
Insufficient sleep Sleep disordered breathing - OSA, CSA, hypoventilation, etc. Central Sleep disorders-Narcolepsy, Kleine-Levin syndrome, Idiopathic hypersomnelence. Circardian rhythm sleep disorders Sleep related movement disorders Parasomnias- RBD, sleep walking, sleep terrors, confusional arousals. Neurologic disorders - Parkinson's, dementia, stroke, MS Medical: -Hypothyroidism , Adrenal insufficiency , Anemia, iron deficiency , CKD, renal failure, hepatic encephalopathy Depression, other psychiatric conditions Medications, substances
117
What medical conditions should make you think about screening for OSA?
OHS Difficult to control HTN Recurrent atrial fibrillation post cardioversion or ablation Pulmonary Hypertension
118
Neurological control of upper airway muscles
Cranial nerves 5,7,9,10,11,12
119
Risk Factors for OSA
Smoking Elevated BMI Family history Increased age Male, post menopausal Increased mallampati score Tonsil or adenoid hypertrophy Increased neck circumference Retrognathia Micrognathia Macroglossia Nasal abnormalities Low lying palate Hypothyroidism Acromegaly Neuropathy or myopathy
120
Mechanism of hypoxemia in OSA
Underlying lung disease Baseline supine SaO2 Low FRC (e.g. obesity) Duration of apneic/hypopneic episodes Frequency of apneic /hypopneic episodes Respiratory efforts in between apneic/hypopneic episodes
121
Possible complications of OSA
Hypertension Coronary artery disease Arrhythmias Stroke Heart failure PH if concomitant OHS Diabetes Erectile dysfunction Depression Cognitive deficits MVCs
122
Screening questionnaires for OSA
Berlin questionnaire STOP-Bang questionnaire (high sensitive, poor specificity)
123
Diagnostic criteria for OSA
Symptoms/complications + AHI >/5 AHI >/15
124
Severity of OSA
Mild: >/5 - 14.9 Moderate: 15 - 29.9 Severe: >/30
125
Positional sleep apnea definition
Supine AHI is at least double non supine AHI
126
Indications for PAP treatment in OSA
Moderate to severe OSA/ AHI >/15 Mild but symptoms (e.g. EDS), reduced QOL, or hypertension Critical occupation
127
Starting pressure and max pressure for PAP
Start at 4 cm H2O Switch to BPAP 15 cm H2O Absolute max 20 cm H2O
128
Min and max pressures for BPAP
Min difference of 4 cm H2O Max difference of 10 cm H20 Min pressure 4 cm H2O, Max pressure of 30 cm H2O
129
How to progress titrating to next pressure during titration study
>/2 apneic events >/3 hypopneic events >/5 RERAs >/3 mins snoring Any of this within a 5 min period Want >/ 30 mins without breathing event
130
Criteria for optimal titration achieved
1. Optimal: RDI <5 for at least 15 mins, supine sleep observed, REM sleep not interrupted by spontaneous arousals, O2 sat >90% 2. Good: RDI 90% 3. Adequate: RDI not 90% 4. Unaccepted: None of the above are met
131
Causes of persistent sleepiness in OSA despite treatment
Non adherence/compliance Additional medical condition Additional sleep disorder Treatment emergent central sleep apnea Inadequate pressures/not fully controlled Sleep deprivation/insufficient sleep
132
Once the other causes are ruled out, how can you treat patients with OSA who still have EDS?
Modafinil Solriamfetol
133
Indications for modafinil in OSA
Ongoing EDS despite appropriate treatment Concomitant narcolepsy Concomitant circadian rhythm disorder Certain occupations - shift workers (Temporary)
134
Methods to increase adherence to PAP therapy
Education Humidity Nasal mask vs. full face mask Treatment of nasal congestion Polypectomy Oral appliance APAP
135
Benefits of treatment (PAP, OA, MMA)
Improved AHI (all stages) Improved symptoms: Definitely moderate-severe, unclear mild Decreased BP: moderate-severe PAP also improves responsiveness of Afib to tx, ?improve outcome after stroke
136
Contraindications to APAP
Chronic lung disease e.g. COPD Previous UPPP (Uvulopalatopharyngoplasty) Heart failure Central sleep apnea OHS/hypoventilation syndrome Medications causing hypoventilation e.g. chronic opioid use Neuromuscular disease, chest wall disorder
137
Treatments for OSA other than PAP
Positional therapy Oral appliances Surgery Hypoglossal nerve stimulation Weight loss
138
Indications for oral appliance
Primary snoring disorder without OSA OSA but intolerant of or unwilling to try PAP (vs. no treatment) To reduce PAP pressures Not responsive to CPAP
139
Complications associated with OA
Dental malocclusion TMJ pain Gum pain Drooling or dry mouth
140
Surgical options in OSA
UPPP (Uvulopalatopharyngoplasty) Mandibular advancement Tonsillectomy, adenoidectomy Tracheostomy
141
Reasons to consider tracheostomy for sleep disordered breathing
Intolerant of PAP/high pressures Cannot achieve control with other treatment Other abnormalities prevent adequate mask fitting Other reasons for tracheostomy e.g. craniofacial weakness Patient preference
142
Main things you should assess on overnight oximetry
Mean nocturnal saturation (92) Nadir SpO2 Time spent
143
Cutoffs for the Oxygen Desaturation Index
<10 = unlikely moderade-severe OSA 10-30 = possible moderate-severe OSA >30= highly suggestive of moderate-severe OSA but technically <5 is normal and >10 is abnormal
144
What are the abnormal hypoxemia times on an overnight oximetry
Spo2 <88% for >5min Spo2 <90% for >10% of sleep time.
145
What is considered an oxygen desaturation for an ODI?
Reduction in SpO2 >/4% for >/10 seconds
146
Components of insomnia
Difficulty sleeping or maintaining sleep Adequate opportunities for sleep Affect functioning
147
PSG findings of insomnia
Increased WASO Increased sleep latency >/30 minutes Reduced sleep efficiency Reduced sleep time <6-6.5 hours
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Medical causes of insomnia
Medications e.g. stimulants, coffee Psychiatric e.g. depression, anxiety Neurologic e.g. parkinsons, dementia Chronic pain, diabetes, HTN, cancer
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Classification of central sleep apnea
1. Primary central sleep apnea 2. Primary central sleep apnea of infancy or prematurity 3. CSA with Cheyne stokes 4. CSA due to medical disorder without Cheyne Stokes - 4a. Central insult e.g. tumour, stroke, encephalitis, polio - 4b. Respiratory muscle weakness e.g. NMD, chest wall disease - 4c. Renal failure - 4d. Atrial fibrillation 5. High altitude periodic breathing 6. Treatment emergent central sleep apnea 7. Medication or substance related
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Medications that can cause CSA
Opioids Benzodiazepines Gabapentinoids Antidepressants
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PSG findings in general CSA
Cessation or reduction in ventilatory effort x >/10 seconds Most common in N1/N2 No effort via RIP belt or diaphragmatic EMG >/5 central events per hour and >50% of total events Snoring and desats are less prominent than OSA
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PSG definition of Cheyne Stokes Respiration
1. - >/3 consecutive central apnea/hypopneas with crescendo and decrescendo changes in breathing amplitude with a cycle length of at least 40 seconds (typically 45 to 90) 2. - >/5 central apneas/hypopneas per hour associated with crescendo,decrescendo breathing in between recorded over min 2 hours
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Diagnostic criteria of Cheyne Stokes Respiration (CSR)
Symptoms/predisposing condition (HF, neurologic dz, AF) PSG criteria Not better explained by other disorder
154
Cheyne Stokes Respiration vs. Central Sleep Apnea
Cycle length longer >40 seconds Period of hyperpnea is longer O2 saturation nadir is more delayed (prolonged circulation time) Arousals during hyperpnea whereas at end of apnea with CSA
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Causes of Cheyne Stokes Respiration
Heart failure Renal failure Central disease e.g. stroke, tumors Medications e.g. sedatives
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Pathophysiology of Cheyne Stokes Respiration
1. Apnea 2. Increased circulatory time 3. Increased chemoreceptor responsiveness to CO2 4. Increased loop gain - increase in response size 5. Apnea
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Pathophysiology of other CSAs
TECSA: obstruction relieved, CO2 falls, apnea, high loop gain (treatment emergent central sleep apnea) Altitude: increased vent due to O2, CO2 falls, apnea, high loop gain Opioids: hypoventilation
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Impact of CSR on HF
Increased mortality Occurs in 30% of patients with HF
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Treatment options for CSR
GDMT of HF, transplantation Nocturnal oxygen CPAP therapy - (not the other OSA tx) - BPAP used with caution bc can have same effect as ASV, so avoid Phrenic nerve stimulation ?Acetazolamide, theophylline [limited evidence]
160
Benefits of CPAP in CSR
Improve AHI Improve arrhythmias May improve LV function
161
SERVE-HF trial
adaptive servoventilation (ASV) increased all cause mortality in HFrEF <45% Contraindicated
162
Management of general CSA
Idiopathic → BPAP-ST, ASV, CPAP CSA 2/2 hypoventilation → BPAP-ST, ASV > CPAP Altitude → descend, oxygen, acetazolamide Treatment emergent → expectant, ASV > BPAP-ST, oxygen, acetazolamide
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Biot’s breathing
Hyperpnea mix with apnea Associated with meningitis
164
Changes that occur to the sleep architecture with altitude
Increased WASO (Wakefullness after sleep onset) Increased N1, N2 Decreased N3 Kind of like aging
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Mechanism of action of acetazolamide
Carbonic anhydrase inhibitor Leads to increased bicarbonate excretion Causes metabolic acidosis, stimulates breathing
166
Classification criteria for sleep related hypoventilation (types of hypoventilation)
Idiopathic central alveolar hypoventilation syndrome Congenital central alveolar hypoventilation syndrome Obesity hypoventilation syndrome Sleep related hypoventilation due to disorder, medication, substance
167
Cause of congenital central hypoventilation syndrome
Autosomal dominant PHOX2B gene mutation → loss of RTN Also known as Ondines Curse
168
Role of obesity in OHS
Fat produces more CO2 Leptin suppresses respiratory drive Altered respiratory mechanics(TLC N/**reduced at BMI>40,** **FRC reduced**, RV normal/increased, RV/TLC normal/increased, **ERV low**, ).
169
Indications for screening for OHS
BMI >30 with OSA (known or suspected) BMI >30 with: - Unexplained dyspnea - Unexplained awake hypoxemia - Pulmonary hypertension, signs of it - Polycythemia, sx of it (e.g. facial plethoraX) - Elevated bicarbonate
170
How do you screen for OHS?
Bicarbonate >27 Straight to PaCO2 if high pretest probability
171
Diagnostic criteria for OHS
BMI >30 Awake PaCO2 >45 Hypoventilation not explained by another disorder e.g. lung disease (PSG is required to assess for OSA, not absolutely needed for diagnosis but almost always done)
172
Treatment of OHS
AHI >30 → CPAP first AHI <30 → BIPAP-ST No OSA → BiPAP-ST Weight loss (25-50%), not sole treatment If admitted with resp failure → BIPAP-ST> APAP until sleep study
173
Treatments that are associated with HARM in the management of OHS
Oxygen Respiratory stimulants
174
Classification criteria for hypersomnolence
Primary - Idiopathic hypersomnia - Kleine Levin syndrome - Narcolepsy Secondary - Genetic disorder - CNS disorder e.g. stroke - Parkinsons - Post traumatic - Metabolic encephalopathy
175
DDX of Sleep Onset REM Periods
Narcolepsy Idiopathic hypersomnolence Due to PD, post traumatic, genetics, central tumour, metabolic REM rebound: - Depression - Medication withdrawal e.g. SSRIs, BZD, alcohol - REM sleep deprivation - Patients undergoing CPAP titration
176
Requirement prior to MSLT
PSG the night before (NOT split night) >/ 6 hours of sleep on PSG Withhold REM suppressing medications x 2 weeks
177
Causes of narcolepsy
Idiopathic Autoimmune, post infectious Neurosarcoid CNS - strokes, tumors
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Features of narcolepsy
Sleep attacks during the day and EDS Hypognogic Sleep paralysis +/- cataplexy
179
PSG/MSLT features of narcolepsy
Mean sleep onset latency /2 SOREMPs
180
Drug categories used in treatment of narcolepsy
Selective DA reuptake inhibitor - Modafinil Selective NE and DA reuptake inhibitor - Methylphenidate - Solriamfetol DA reuptake inhibitor - dextroamphetamine H3 blocker - pitolisant Other - Sodium oxybate: GHB - Venlafaxine for cataplexy
181
Conditions that are associated with REM sleep behavior disorder
Parkinsons MSA, other forms of dementia Stroke, tumour Narcolepsy SSRIs
182
Treatment for REM sleep behavior disorder
Changes to make sleeping area safe Melatonin Clonazepam
183
Sleep disorders can occur secondary to Parkinsons Disease
Insomnia Hypersomnolence REM sleep behavior disorder Restless leg syndrome Excessive daytime sleepiness
184
Examples of opioid related disorders
Central sleep apnea Hypoventilation Obstructive sleep apnea Insomnia
185
Causes of RLS
Iron deficiency Pregnancy Uremia Parkinson disease, spinal cord disease, prolonged immobility SSRIs + other meds Family history Thyroid dysfunction
186
Scoring a PLM (periodic leg movement)
4 consecutive flexion movements, 5-90 s apart is a series (counts as 1). The movement is 0.5-10 s, 8mV in amplitude above resting EMG Can't be during a resp event.
187
Diagnosis of PLMD (periodic leg movement disorder)
Periodic leg movement index (PLMI) >/15 per hour Not explained by another cause e.g. other sleep disorder
188
Diagnostic criteria for RLS
Urge to move limbs Rest worsens symptoms Getting up/moving relieves Evenings/Night are worse Dysfunction (causes concern) (URGE-D)
189
Treatment of RLS
Iron replacement -if serum ferritin <75ng/mL or TSAT <20% IV or oral iron supplementation -If serum ferritin 75-100 then only IV iron -If ESRD then use IV iron Sucrose when ferritin <200 and TSAT <200 -IV ferric carboxymaltose (strong recommendation) can use IV LMW iron dextran, IV ferumoxytol, ferrous sulfate, but conditional recommendations Alpha-2-delta calcium channel ligands (Strong recommendation) -gabapentin -gabapentin encarbil (long acting gabapentin) - pregabalin Opioids Peroneal nerves stimulation Dipyridamole Vitamin C if ESRD DO NOT USE: Gabapentinoid - pregabalin, gabapentin DA agonist - pramipexole, ropinirole DA analogue - carbidopa-levodopa
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Examples of circadian rhythm disorders
Advanced sleep- wake phase Disorder (light therapy) Delayed sleep phase wake phase Disorder (melatonin) Irregular sleep-wake rhythm disorder (light therapy and no sleep aids for elderly. For younger patients=melatonin) Non 24H Sleep wake rhythm disorder (Strategic melatonin in blind patients) Caused by inbalance between process C and S
191
Criteria for sleep related hypoxemia
SpO2
192
What innervates the respiratory muscles?
Diaphragm - C3/4/5 Intercostals - thoracic nerves Abdominal - lumbar nerves Upper airways - cranial nerves
193
Levels of neuromuscular disease and diseases associated
Cerebral cortex - stroke, cancer Brain stem/basal ganglia - stroke, cancer Spinal cord - trauma, MS Anterior horn cell - polio, post polio, ALS Motor nerves - ALS NMJ - MG, LEMs Muscles - muscular dystrophy (duchenne and becker)
194
DDX for elevated Residual Volume
ALS Mid-low c-spine injury airways disease
195
DDX for low ERV
Obesity T spine injury pregnancy
196
Measures of respiratory muscle strength
Sitting and supine VC MIP, MEP SNP Sniff esophageal pressure Phrenic nerve EMG Sniff transdiaphragmatic pressure
197
Clinical manifestations of ALS
Bulbar symptoms UMN symptoms: spasticity, hyperreflexia, extensor plantar LMN: atrophy, fasciculations
198
Causes of nocturnal hypoxemia in ALS
Concomitant OSA (?CSA, mixed>OSA) Concomitant hypoventilation - resp muscle weakness Central hypoventilation (loss of cortical drive to breath) Underlying lung (e.g. VQ mismatch due to microatelectasis), heart, PVD disease Upward shift in ventilatory setpoint for PaCO2 by 2-3 mmHg
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In hypoventilation due to muscle weakness, what is the progression of symptoms?
REM → NREM → daytime Loss of accessory muscles in REM
200
What Monitoring every 2-6 months in ALS
Clinical symptoms FVC sitting Supine FVC, MIPS, MEPS, SNPs Cough hx, PCF Arterial blood gas/TcCO2 if hypercapnia suspected, or bulbar sx preclude PFT Nocturnal oximetry/PSG if SDB suspected
201
Indications to start NIV in ALS
Orthopnea FVC <50% predicted (Upright reliable<65% Canadian Best Practice 2020) Sitting or supine FVC <80% predicted with sx and other indicator of resp muscle weakness MIPS or SNPS <-40 cm Daytime PaCO2 >45 mmHg Abnormal nocturnal oximetry or symptomatic Sleep disordered breathing: - Sleep disordered breathing as defined by oxygen saturation < 90% for > 5% of the night or < 88% for 5 consecutive minutes or a 10 mmHg increase in TcCO2 during sleep AND any of the following symptoms: dyspnea, morning headache, daytime sleepiness, or non-refreshing sleep.(CTS 2019) *Start with S/T mode over S mode (CTS 2019)
202
Best predictors of death at 6 months in ALS
FVC <50% predicted SNP <-40 MIP <-40
203
Benefits of NIV in ALS
HrQOL Some physiological parameters e.g. slowing VC decline, daytime PaCO2 Mortality
204
What does not yet have a clear goal in ALS treatment?
Respiratory muscle training Diaphragmatic pacing
205
Benefits of tracheostomy in ALS
HrQOL Mortality
206
Medications should be avoided in myasthenia
Fluoroquinolones Aminoglycosides Macrolides Beta blockers Procainamide Checkpoint inhibitors Iodinated contrast
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Treatment of MG
Maintenance - pyridostigmine Flare - steroids, PLEX, IVIG
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Lambert Eaton Syndrome vs. MG?
More proximal muscle weakness More ANS abnormalities Less bulbar muscle involvement
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Respiratory risks/manifestations associated with GBS
Weak cough Bulbar dysfunction - Aspiration pneumonitis, aspiration pneumonia Respiratory muscle weakness - hypoventilation, atelectasis Sleep disordered breathing Dysautonomia and bronchospasm
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Predictors of respiratory failure in GBS requiring mechanical ventilation
FVC <60% predicted Onset to admission <7 days Inability to stand, life arms up, life head off pillow Presence of facial weakness Inability to cough
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Indications for intubation in GBS
20-30-40 rule (each as separate point) : VC<20 MIP < -30 MEP < 40 Severe bulbar weakness, cannot protect airway Respiratory rate sustained >30 Hypoxemia/SpO2 <92% Hypercarbia >50mmHg Hemodynamic instability
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Treatment of GBS
IVIG, PLEX
213
What are the types of muscular dystrophy?
BMD (Becker) DMD (Duchenne)- worse
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Predictors of nocturnal hypoventilation in muscular dystrophy?
VC <40% in DMD VC <60% in other muscular dystrophies Therefore, screening PaCO2 in those with VC <40%
215
What are causes of unilateral vs bilateral diaphragmatic paralysis?
216
Most common cause of unilateral hemidiaphragm
Trauma Idiopathic
217
Clinical manifestations of diaphragmatic paralysis
Exertional dyspnea Orthopnea Bendopnea Sleep disordered breathing symptoms
218
Physical examination findings in diaphragmatic paralysis
Paradoxical motion in unilateral Paradoxical abdominal wall retraction
219
Diagnostic tests to assess for paralysis
Imaging Sniff test - ultrasound, fluoroscopy Sitting and supine test MIP, SNP EMG of diaphragm, transdiaphragmatic pressure
220
Values of MEP/MIP that are concerning for diaphragmatic paralysis
MEP/MIP >1.5 for unilateral MEP/MIP >3 for bilateral
221
Complications of diaphragmatic paralysis
Unilateral: occasional hypoventilation, atelectasis Bilateral frequent hyperventilation, atelectasis, PNA, resp failure
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Treatment of diaphragmatic weakness
Unilateral: plication Bilateral: NIV, pacing
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Indications for NIV for NMD in general
* FVC < 80% associated with symptoms such as tachypnea and use of accessory muscles, tachypnea, excessive fatigue, excessive daytime sleepiness * SNIP < 40 mmHg * MIP < 60 mmHg (?<40 ALS) * Daytime hypercapnia PCO2 > 45 mmHg * Nocturnal saturation < 88% for 5 consecutive minutes
224
Causes of kyphoscoliosis
Idiopathic Congenital - spinal/vertebral malformations at birth Cartilage disorders - Marfan syndrome, EHD Bony disorders - e.g. osteopenia, osteoporosis Neuromuscular disorders - e.g. muscular dystrophy, cerebral palsy, Charcot Marie Tooth Post thoracoplasty
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Risk factors for respiratory failure in kyphoscoliosis
Cobb’s angle >110 degrees VC <45 degrees in surgically untreated (we start monitoring at VC <50%) Concomitant NMD Concomitant lung disease
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Screening for NIV needs in patients with kyphoscoliosis
Once FVC <50%, we look for hypercapnic resp failure
227
Treatment of respiratory failure in kyphoscoliosis
Nocturnal NIV +/- O2 Nocturnal O2 if just hypoxemia
228
Benefits of airway clearance
Secretion clearance Reduce airway resistance Improve respiratory system compliance Prevent atelectasis Prevent pneumonia Prevent respiratory failure, prevent need for trach or intubation Decrease work of breathing
229
Markers of a weak cough
PCF <270 L/minute MEP <60 cm H2O Bulbar dysfunction Expiratory cough flow tracing - absence of transient increase in expiratory flow (cough spikes)
230
Secretion management strategies in DMD
Atropine Scopolamine Botox injection into salivary glands (submandibular and parotid) Salivary gland RT
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Indications to start a cough support device in NMD
PCF <270 L/minute
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Methods to enhance cough in NMD
Lung volume recruitment - glossopharyngeal breathing, bag valve mask Manually assisted cough Mechanical insufflation and exsufflation device
233
Contraindications to lung recruitment in NMD
Unconscious or unable to communicate Increased ICP, severe TBI SIgnificant hypotension Pneumothorax, risk for barotrauma e.g. bullous disease Hemoptysis ?Cannot protect their airway e.g. severe bulbar weakness
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Contraindications to NIV
Loss of consciousness, unable to protect airway Requiring intubation Hemodynamic instability Facial trauma or deformity Hemoptysis Upper GI bleeding, perforation or recent surgery
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Causes of hypercapnia in patient with NMD on BPAP?
Non compliance or low duration Pressures are not optimal Disease progression Underlying lung disease Compensation for metabolic alkalosis
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Other than BiPAP, other ways to optimize respiratory status in NMD
Cough assist Secretion mobilization and volume Daytime mouthpiece ventilation Smoking cessation Vaccination
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DDX for a lymphocyte predominant BAL pattern
Lymphoproliferative disorders Connective tissue diseases Cryptogenic organizing pneumonia Radiation pneumonitis Sarcoidosis Hypersensitivity pneumonitis NSIP Drug induced pneumonitis
238
DDX for an eosinophilic predominant BAL pattern
Infections - fungal, PJP, helminthic ABPA Hodgkin’s lymphoma Eosinophilic pneumonia Asthma, bronchitis EGPA Drug induced pneumonitis Bone marrow transplant
239
DDX for a neutrophil predominant BAL pattern
Infection Bronchitis Aspiration pneumonia UIP/IPF Asbestosis ARDS, DAD Connective tissue diseases
240
What BAL value of lymphocytes is suggestive of granulomatous inflammation?
>25% >50% is especially suggestive of HP or cellular NSIP
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Pulmonary manifestations of drug induced disease
Eosinophilic pneumonia Hypersensitivity pneumonitis Organizing pneumonia Occupational asthma Diffuse alveolar hemorrhage ARDS Drug induced sarcoid reaction, vasculitis and lupus Bronchiolitis - obliterative bronchiolitis Fibrosing mediastinitis Pleural effusions Pulmonary hypertension Alveolar hypoventilation
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RFs for development of amiodarone induced lung toxicity
Older age >/2 months of therapy >/400 mg oral daily Total cumulative dose High FiO2 administration Underlying lung disease
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RFs for development of bleomycin induced lung toxicity
Older age Cigarette smoking Higher doses (>400 units) Concomitant radiation Concurrent cisplatin or cyclophosphamide High FiO2 administration Underlying lung disease
244
RFs for development of nitrofurantoin lung toxicity
Older age Female Renal impairment
245
Medications that cause mediastinal lymphadenopathy
Phenytoin Methotrexate
246
Benefits of O2 therapy in ILD
Resting hypoxemia: dyspnea, QOL, ?PH Ambulatory hypoxemia: Exercise tolerance
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DDx for ILD with preserved lung volume
CPFE* Chronic sarcoidosis* Chronic HP* RB-ILD* LAM PLCH Lymphangitic carcinomatosis Heart failure
248
General Approach to DDx of radiographic patterns in ILD
249
Definition of honeycombing
Clustered cystic airspaces, 3-10 mm in diameter with walls 1-3mm thick usually subpleural
250
Reticular Pattern Definition
Small linear opacities with intra and interlobular thickening
251
Ground Glass Definition
Hazy increased lung opacity with preservation of bronchial and vascular markings
252
Consolidation Definition
Increased attenuation that obscures the margins of vessels and airways
253
Cyst Definition
Well defined focal lucency with variable wall thickness bust usually thin (less than 2mm)
254
Micronodule Definition
small round focal opacity <3mm in size
255
Mosaic Attenuation Definition
Patchwork of regions of differing attenuation
256
Outline the components of a secondary pulmonary lobule.
257
Important studies in the treatment of ILD
INPULSIS 1 and 2: nintedanib in ILD (Primary outcome: annual change in FVC * INPULSIS-1: 125.3 ml/year * INPULSIS-2: 93.7 ml/year Myocardial infarcts: * higher incidence in Nintedanib group 1.5% vs 0.5% * MACE 0.6% nintedanib vs 1.8% placebo Kolb et al. Thorax 2017 (nintedanib) * IPF and preserved lung volume FVC >90% Same rate of lung function decline Same benefit Start early! Less risk of exacerbations ASCEND: Pirfenidone in ILD Primary outcome: * >/= 10% decline in FVC or all cause mortality * 16.5% vs 31.8% (RRR 47.9%; P<0.001; NNT 7) (Mortality benenifit not proven but subsequent metanalysis do support that there is a mortality benefit) SENSIS: Nintedanib in SSc-ILD INBUILD: Non IPF fibrosing ILD PANTHER: Steroids had increased mortality in IPF
258
Numerical cutoffs for surgical lung biopsy
FVC <55% DLCO <35%
259
Possible adverse events post surgical lung biopsy
Prolonged air leak Pneumothorax, hemothorax, pleural effusion Infection Delayed wound healing ILD exacerbation Requirement for intubation
260
Benefits of PR in ILD
Improved dyspnea Improved QOL
261
Management of refractory dyspnea in ILD
Breathing retraining Relaxation techniques Fans Body positioning Low dose opioids
262
RFs for IPF
Genetics - TERC/TERT/MUC5B Smoking Environmental pollution ?Microaspiration
263
Definitions of familial pulmonary fibrosis
Fibrotic ILD in at least 2 related family members
264
Conditions are associated with UIP pattern
IPF Familial IPF CTD-ILD (SARD- ILD) Drugs Asbestosis Chronic hypersensitivity pneumonitis
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Radiographic pattern of UIP + associated level of confidence
Confident - 90% Probable - 70 to 90 Indeterminate - 50 to 70 Alternative - <50%
266
Mediastinal findings that would suggest an alternative diagnosis to UIP
Esophageal dilatation Pleural plaques
267
Type of biopsy is recommended for IPF
Surgical lung biopsy Cryobiopsy
268
Histopathological findings in IPF
Subpleural and/or paraseptal predominance Patchy involvement Dense fibrosis with architectural distortion +/- honeycombing Fibroblastic foci Absence of features suggesting alternative diagnosis e.g. granulomas
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Poor IPF prognostic factors on initial diagnosis
Older age Male FVC <50% DLCO <35% Greater extent of fibrosis on CT Hypoxemia at rest or with exertion Low 6MWT, especially <250 meters Lower BMI Certain comorbidities e.g. PH
270
Poor IPF prognostic factors on follow up
Absolute reduction in FVC by 10% Absolute reduction in DLCO by 15% Worsening fibrosis on HRCT Worsening level of dyspnea
271
Poor UIP prognostic factors
IPF as opposed to secondary dx Male Older age Heavy smoking Poor baseline FVC Poor baseline DLCO Decline in FVC by 10%, DLCO by 15% over 6 months CPFE PH
272
“Appropriate clinical setting” for IPF?
Male Smoker >60 years old
273
Comorbidities that need to be managed in IPF
GERD Pulmonary hypertension Obstructive sleep apnea Lung cancer
274
Therapies that improve survival in IPF
Antifibrotics: nintedanib and pirfenidone Lung transplantation
275
Benefits of antifibrotics
Improve QOL Reduce the decline of FVC Reduce rate of exacerbation and hospitalization Reduce the mortality
276
Requirements for antifibrotic initiation/who would benefit
Age >40 FVC >/50 DLCO >/30
277
Overall prognosis for IPF
Death within 4-5 years of diagnosis
278
Possible triggers for an IPF flare
Bad disease at baseline - low FVC, DLCO, 6MWD Infection Pulmonary embolism Aspiration Lung biopsy, bronchoscopy, other procedures Immunosuppressive therapy
279
Prognosis of an IPF flare
50-90% in hospital mortality Median survival 3-4 months
280
Diagnostic criteria for IPF flare
Acute respiratory deterioration <1 month in duration Bilateral GGO with or without consolidation on background of fibrosis Not explained fully by another cause e.g. volume overload
281
Criteria for progressive pulmonary fibrosis
Need two of the three criteria Need them to be occurring in the past year 1. Progression of symptoms 2. Decline in PFTs - FVC >5% within one year - DLCO >10% within one year 3. Worsening radiographic progression
282
DDX of PPFE (pleuroparynchymal fibroelastosis)
Idiopathic CTD e.g. scleroderma Chronic HP Occupational exposures Chemotherapy Post HSCT, bone marrow, lung
283
Imaging findings in PPFE
Pleural thickening Associated subpleural fibrosis Concentrated in the upper lobes
284
Histopathological findings in PPFE
Upper zone pleural fibrosis Subjacent intra alveolar fibrosis and alveolar fibroelastosis
285
Radiographic findings of CPFE
Emphysema in upper lobes Fibrosis (usually UIP pattern) in lower lobes
286
Notable complications of CPFE
Lung cancer Pulmonary hypertension
287
Diagnostic criteria for IPAF
Presence of interstitial pneumonia (imaging or pathology) Does not meet CTD criteria Exclusion of other etiologies At least 2 of: clinical criteria, serological criteria, morphological criteria
288
Secondary causes of NSIP
Idiopathic Connective tissue diseases Drugs/medications Exposures - hypersensitivity pneumonitis Infections, including HIV
289
Radiographic features of NSIP
Basilar, peripheral OR diffuse Cellular is GGO dominant Fibrotic is reticulation, traction, bronchovascular bundle thickening +/- honeycombs Subpleural sparing
290
General Pathology findings for UIP, NSIP, OP, fHP, and PPFE
UIP→ fibroblastic foci, honeycombing NSIP→ homogenous fibrosis, no Honey Combing, few fibroblastic foci OP→ MASSON bodies (buds of intraalveolar granulation tissue) Fibrosing HP→ poorly formed granulomas, peribronchiolar, SHAUMANN bodies PPFE→ fibroelastosis, spindle cells.
291
Causes of drug induced sarcoidosis
TNF alpha inhibitors Immune checkpoint inhibitors HAART Interferons
292
Pulmonary manifestations of sarcoidosis
Interstitial lung disease Progressive massive fibrosis Alveolar sarcoid Tracheal stenosis, subglottic stenosis Lower airway obstruction Lymphadenopathy Pulmonary hypertension
293
Mechanisms of PH in sarcoidosis
Interstitial lung disease Cardiac disease e.g. cardiomyopathy PVOD like lesions Granulomatous inflammation and involvement of vessels → intrinsic sarcoid vasculopathy Fibrosing mediastinitis External compression of PA by lymphadenopathy Portal hypertension
294
Non pulmonary manifestations of sarcoidosis
Neuro - hydrocephalus, aseptic meningitis, facial nerve palsy, small fiber neuropathy, optic neuritis, encephalopathy, psychosis Ocular sarcoidosis - anterior uveitis Cardiac sarcoid - cardiomyopathy, heart block, arrhythmias Renal sarcoid - nephrolithiasis Hepatic sarcoid - transaminitis, cholestasis Hypercalcemia, hypercalciuria Rashes Other: spleen, bone marrow
295
Clinical features that make diagnosis of sarcoidosis highly probable
Uveitis Optic neuritis Lofgren’s syndrome Lupus pernio Erythema nodosum Hypercalcemia or hypercalciuria Bilateral hilar adenopathy Perilymphatic nodules Gadolinium enhancement Parotid uptake Osteolysis, cysts/punched out lesion
296
DDX for erythema nodosum
Medications e.g. OPC, TNF alpha inhibitors Infections e.g. hepatitis B, streptococcus, fungal Inflammatory e.g. sarcoidosis, IBD Malignancy Pregnancy
297
How does small fiber neuropathy present?
Paresthesias Numbness Pain Autonomic dysfunction - palpitations, orthostasis, sexual dysfunction
298
How is Erdheim Chester syndrome differentiated from sarcoidosis?
BRAF V600 somatic mutation CD68 marker on biopsy Also is from proliferation of foamy histiocytes rather than granulomas
299
Pulmonary manifestations of IgG4 disease
Lymphadenopathy Nodules or masses Interstitial lung disease Fibrosing mediastinitis Subglottic stenosis, tracheal stenosis Pleural thickening Pleural effusions
300
Diagnosis of IgG4 disease
Serum and BAL IgG4 can be suggestive Biopsy definitive
301
Manifestations of cardiac sarcoidosis
Conduction e.g. AV block, BBB, tachyarrythmias, sudden death Cardiomyopathy Coronary artery disease from vasculitis
302
How do you investigate cardiac sarcoidosis?
Cardiac MRI (ATS suggests this first line) Cardiac PET Transthoracic echocardiogram
303
Lab findings in sarcoidosis
Anemia, thrombocytopenia, leukopenia Hypergammaglobulinemia Hypercalcemia, hypercalciuria Elevated rheumatoid factor
304
DDX for elevated serum ACE
Sarcoidosis Hypersensitivity pneumonitis Silicosis Berylliosis Asbestosis Tuberculosis Coccidioidomycosis Hodkin’s lymphoma Gaucher’s disease (lysosomal storage disorder caused bya deficiency in the enzyme glucocerebrosidase leading to the accumulation of glucocerebroside in tissues) Hyperthyroidism PBC
305
Imaging findings in sarcoidosis
Perilymphatic distribution of nodules Miliary nodularity Lymph node enlargement, can have eggshell calcification Galaxy sign (small nodules surrounding larger conglomerate masses) Garland sign (bilateral hilar lymphadenopathy and right paratreacheal lymphadenopathy) Progressive massive fibrosis Signs of fibrosis - reticulation, traction, volume loss Alveolar sarcoidosis Lambda sign (bilateral hilar lymphadenopathy and right paratreacheal lymphadenopathy but lights up on a gallium 67 scan) Panda sign (parotid uptake)
306
Patterns of calcification often seen in sarcoidosis LN
Eggshell Icing sugar
307
Cutoffs for CD4-CD8 count for sarcoid
<1 → highly unlikely >4 → highly likely
308
Staging criteria for sarcoidosis ( and spontaneous remission %)
I: LN → 90% II: LN and parenchymal changes → 70% III: parenchymal changes →20% IV: fibrosis → 0%
309
Diagnosis of sarcoidosis
If lofgrens or heerfordt no biopsy. If asymptomatic but radiographic findings can do EITHER biopsy OR close follow up. If not confirmed then biopsy (EBUS recommended) Screen with CBC,Cr, ALP (not ALT), Ca, (if Vit D needed do 25 adn 1-25), ECG (not holter or TTE), eye exam
310
Pathological finding in sarcoidosis
Non caseating granuloma Discrete, well organized granulomas composed of giant cells, histiocytes and surrounded by lymphoblasts Granulomas distributed along lymphatics and bronchovascular bundles Sparse surrounding lymphocytic infiltrate
311
Difference between HP and sarcoidosis pathology
Non caseating granulomas in both Poorly formed, small, loosely arranged in HP Distribution around bronchioles in HP vs. perilymphatic in Sarcoid Inflammatory infiltrates found at interstitial sites distant from granuloma. Marked lymphocytosis on BAL in HP and >4CD4/CD8 ratio in sarcoid
312
Who can forgo lymph node sampling in suspecteted sarcoid?
Heerfordt’s syndrome Lofgren’s syndrome Lupus pernio (blue red to violet smooth shiny nodules and plaques on the head and neck, predominantly on the nose, ears, lips, and cheeks)
313
DDX for non caseating granulomas
Sarcoidosis Sarcoid like reactions to malignancies Lymphoma Hypersensitivity pneumonitis Berylliosis IgG4 disease PLCH Erdheim Chester disease GI diseases e.g. PBC, IBD
314
DDX for usually necrotizing granuloma
Tuberculosis, fungal infections, syphilis Vasculitis Rheumatoid nodules GLILD Bronchocentric granulomatosis
315
Sensitivity and specificity of biopsies in sarcoidosis
Endobronchial - 70% sensitive EBUS - 80% sensitive; highest yield Transbronchial- 30-50%
316
RFs for difficult to treat sarcoidosis
African american Age >40 Progressive pulmonary involvement Neuro, cardiac, eye involvement
317
Good prognostic indicators of sarcoid
Erythema nodosum Lofgren’s syndrome Stage I disease Spontaneous improvement or resolution
318
Benefits of treatment in sarcoid
Improve sx/accelerate remission Improve imaging Increases risk of recurrence
319
Things need to be screened at baseline in sarcoid
CBC Crea ALP Calcium ECG Eye examination
320
Things need to be followed up on in sarcoid BW
CBC Crea ALP Calcium
321
Indications for treatment of pulmonary sarcoidosis
Reduced FVC, reduced DLCO Moderate to severe pulmonary fibrosis Precapillary pulmonary hypertension Deterioration in symptoms, lung function or imaging on follow up - as per BTS, DLCO <65% or drop by >/15%, FVC >70%, or drop by >/10%
322
Indications for treatment of extra pulmonary sarcoidosis
Ocular Neuro Renal Hypercalcemia Cardiac
323
Treatment options for sarcoidosis
Glucocorticoids Methotrexate TNF-alpha inhibitors Other: MMF, AZA, lef, JAK inhibitor, rituximab
324
Immune Suppressive Therapies that have RCT level of evidence in sarcoidosis
Steroids MTX Infliximab to improve/preserve FVC and QoL
325
How much steroids do you give them in Sarcoid treatment?
Steroid 20-40 x 4-6 weeks (0.25-0.5mg/kg) evidence 20 as good as 40. Taper 6-18 months
326
Indications to add on second Immune Suppressive Therapy in sarcoid treatment
Progression of disease despite steroids Steroid intolerant Unable to tolerate steroids below 10-15 mg oral daily Strong patient aversion to steroids Presence of major comorbidities made worse by steroids e.g. DM, osteoporosis
327
Agents treat hypercalcemia in sarcoidosis
Steroids Ketoconazole Possibly TNF alpha inhibitors
328
Management of fatigue in sarcoidosis
Exercise training Inspiratory muscle training Methylphenidate, modafinil
329
Treatment of the skin manifestations of sarcoidosis
Topical steroids Oral steroids, MTX (ok evidence) Infliximab* best evidence
330
Treatment of Small Fiber Neuropathy in sarcoid
Symptomatic - gabapentin TNF alpha or IVIG
331
Treatment of neurosarcoidosis
Steroids MTX Infliximab
332
Treatment of cardiac sarcoidosis
Steroids Other IST, but not RCT
333
Poor prognostic variables in cardiac sarcoidosis that would help management decisions
Age >50 Ventricular tachycardia NYHA III-IV LVEF <40% Echo evidence of abnormal global longitudinal strain Interventricular septal thinning Elevated BNP or trop Cardiac inflammation by PET Late gadolinium enhancement by MRI
334
Symptoms that would trigger cardiac work up in Sarcoid
Palpitations Chest pain Syncope, near syncope Tachycardia, bradycardia New ECG findings
335
Vision changes that would trigger a vision work up in Sarcoid
Floaters Blurry vision Visual field loss
336
Who would be “suspected” to have PH in Sarcoid?
Fibrotic lung disease Exertional chest pain Syncope Prominent P2, S4 Reduced 6MWD Desaturation with exercise Increased PA diameter on CT Elevated BNP
337
DDX of dyspnea disproportionate to lung function impairment
Cardiac sarcoidosis Pulmonary hypertension
338
Benefits of steroids in pulmonary sarcoidosis
Improve symptoms (accelerate remission but increase risk of recurrence) Improve or preserve QOL Improve or preserve FVC Improve radiographic disease burden
339
Clinical features are highly suggestive of HP
Female, non smoker Relevant exposure history Hx getting worse with exposure (4-8 hrs), better away. Squawks on examination
340
Poor prognostic markers/increased mortality in HP
Older age Male Smoker Unidentified exposure Ongoing exposure Low FVC, low DLCO Evidence of fibrosis, extent of fibrosis UIP pattern on imaging, histology Fibrotic NSIP pattern Lower BAL lymphocytosis (<20%)
341
Difference of HP from silo filler’s disease and organic dust toxic syndrome
HP is granulomatous disease ODTS and Silo Filler’s disease cause obliterative bronchiolitis
342
Inorganic causes of HP
Isocyanates - spray paints, polyurethane foam, insulation HFA-134a - coolants Drug induced - MTX, bleo, nitro
343
Organic causes of HP
Infectious - Mycobacterium avium, thermophilic actinomyces, aspergillus, bacillus subtilis Animal proteins - bird serum proteins, droppings, feathers Plants - wood dust, flour dust, seaweed
344
Usual lab findings in HP
Lymphocytosis (in BAL) Neutrophilia, lymphopenia Usually no eosinophilia
345
Usual radiographic findings in non fibrotic HP
parynchemal infiltration (GGOs, mosaic attenuation) small airway disease (ill defined centrilobular nodules, air trapping) Distribution (diffuse with possible basal sparing)
346
What are the usual radiographic findings in fibrotic HP
- irregular linear opacities/coarse reticulations with lung distortion (may have some mild traction bronchiectasis and honeycombing) - distribution (random or mid lung zone predominante with sparing in the lower lobes) - ill definied centrilobular nodules/GGOs - 3 density pattern often in lobular distribution
347
Features of pathology for non-fibrotic HP
348
Features of pathology for fibrotic HP
349
Preferred mode of biopsy in HP
Transbronchial in HP Cryobiopsy in fibrotic HP Surgical in both when the others fail
350
When is BAL for assessment of lymphocytosis recommended in HP
Recommended in non fibrotic HP Suggested in non fibrotic HP Depends on ATS vs. Chest
351
Treatment of HP
Observation- Antigen removal Prednisone 0.5 - 1 mg/kg/day x 4-6 weeks then taper over 3 months Steroid sparing agent Antifibrotics
352
Steroid sparing agents that are used in HP
MMF Azathioprine Antifibrotics
353
Normal composition of pleural fluid
75% macrophages 23% lymphocytes 1% mesothelial cells Rare PMNs and eosinophils pH usually 7.6
354
Pressure of the pleura at FRC and at TLC
-5 cm and -30 cm
355
Causes of transudative and exudative effusions
356
What are the 2 and 3 test rules for pleural fluid
Pleural LDH >0.45 ULN Pleural Cholesterol >45 +/- Pleural protein >29 Note light’s (LDH>2/3 ULN, PleurProtein>0.5 SerumProtein, PleurLDH>0.6 SerumLDH)
357
Ddx for eosinophilic pleural effusion.
Blood or air in the pleural space Medications Fungal infections, parasitic infections e.g. paragonimiasis ABPA Malignancies EGPA BAPE PE
358
Ddx for lymphocytic pleural effusion.
Post CABG, PCIS Pseudochylothorax, chylothorax Malignancy (including mesothelioma), lymphoma Tuberculosis Rheumatoid arthritis Sarcoidosis Uremic pleuritis Cardiac failure
359
What is the difference between lymphocytic and very lymphocytic? on BAL
>50% vs >80% Especially TB, lymphoma, RA
360
Ddx for neutrophilic pleural effusion
Empyema Esophageal rupture Acute or chronic pancreatitis Pulmonary embolism SLE can start out neutrophilic TB can start out neutrophilic
361
Causes of low pH/glucose in pleural fluid
Empyema Paragonimiasis RA/SLE effusion Malignancy related effusion Esophageal rupture Hemothorax
362
Causes of elevated pleural protein
Tuberculosis MM, WM
363
How can you tell apart an exudative from pseudoexudative?
P:S albumin <0.6 S-P albumin >12 g/L S-P protein >31 g/L
364
Medication causes of pleural effusion
Methotrexate Nitrofurantoin Amiodarone Phenytoin Ergot alkaloids e.g. bromocriptine Dasatinib Beta blockers
365
DDX for pleural thickening
Benign and malignant masses Pleural infections CTD causes Pleural plaques Post hemothorax Post pleurodesis
366
DDX for pleural calcification
Pleural plaques, previous asbestos exposure Mesothelioma (~20%) Malignancy e.g. extraskeletal osteosarcoma of the pleura Previous radiation Previous infection e.g. TB, empyema Previous pleurodesis Previous hemothorax
367
DDX for positive pleural PET?
Malignancy Infection Autoimmune Previous talc pleurodesis
368
Etiology of fibrothorax
Previous infection, empyema CTD - e.g. RA or SLE related effusion BAPE Previous hemothorax Previous pleurodesis Drug reactions
369
Features of trapped lung
Transudate or borderline exudate fluid Drainage results in pneumothorax ex vacuo Initial (-) intrapleural pressure Pressure falls rapidly bc extremely high elastance No improvement in dyspnea with drainage
370
Management of Hepatic Hydrothorax
Salt and fluid restricted diet Diuresis e.g. furosemide, spironolactone TIPS Transplantation ?Thoracentesis
371
Causes of pleural effusions post CABG
Early post CABG effusion Late post CABG effusion Post cardiac injury syndrome Hemothorax Chylothorax Pneumothorax/hydropneumothorax Parapneumonic effusion Infectious mediastinitis HF related effusion
372
How do you differentiate between early and late nonspecific pleural effusions?
Both are usually left sided Both exudative Early usually bloody, eosinophilic (or neuts) Late usually lymphocytic pH and glucose normal
373
How does PCIS present? (Post Cardiac Injury Syndrome)
Fever, pleuritis, pleural effusion Exudative, lymphocyte predominance Anti myocardial antibodies pH and glucose normal
374
Pleural fluid characteristics of RA
Exudative Glucose <1.6 Pleural to serum glucose <0.5 pH <7.3 LDH >700 Protein >30 Lymphocyte predominant Cholesterol >5.18 mmol/L RF elevated >1:320 C3/C4 reduced Cytology shows multinucleated giant cells (tadpole sign)
375
How is SLE related fluid different from RA related fluid?
More symptomatic - almost always has pleuritis Association with lupus flare More likely to be bilateral Requires tx with NSAIDs or prednisone
376
Causes of chylothorax
Idiopathic Trauma Surgery, especially esophageal Lymphoma, metastatic adenocarcinoma Tuberculosis LAM Yellow nail syndrome Chylous ascites Lymphatic malformations
377
Pleural fluid features of chylothorax
Milky white Exudative Lymphocyte predominant TG >1.24 mmol/L or evidence of chylomicrons (lipoprotein electrophoresis) pH, glucose, LDH normal
378
Pleural fluid features of pseudochylothorax
Milky white Exudative Lymphocyte predominant Cholesterol >5.18 mmol/L or presence of cholesterol crystals
379
Causes of pseudochylothorax
Tuberculosis Helminth infection e.g. paragonimiasis Rheumatoid arthritis Hemothorax
380
Treatment of chylothorax
Dietary changes (low fat, high protein) Fat soluble vitamins Chest tube (unless v small and asx) May need somatostatin/octreotide Sirolimus in LAM Intervention/surgical
381
Triad in yellow nail syndrome
Yellow nails Lymphedema Pulmonary symptoms - sinusitis, bronchiectasis, recurrent PNA, effusions
382
Microbiology of pleural effusions
Staph aureus Strep pneumo GNB (pseudomonas, acinetobacter, klebsiella, enterobacteria) Anaerobic bacteria (baceroides, fusobacterium, etc.)
383
Signs of pleural infection on CT scan
Lentiform shape Split pleura sign (most reliable to differentiate from abscess) Does compress surrounding lung Obtuse angle with the pleura Contrast enhancement Hypertrophy of extrapleural fat
384
If you do not have pleural pH available, what else can you use as guide?
Pleural glucose <3.3
385
Things that affect the clinical outcome (need for sx, mortality) in pleural infections
RAPID score components CT/US septations Pleural contrast enhancement Size >400 cc Pleural fluid microbubbles Increased attenuation f extrapleural fat
386
Things do not affect clinical outcomes in pleural infections
Size of tube Causative organism
387
Components of the RAPID score for pleural fluid evaluation
Renal function (BUN) Age (50-70 or >70) Purulent - yes or no (point if not purulent) Infection source CAP/HAP Diet - Serum albumin
388
What does the RAPID score correspond with?
Mortality at 3 and 12 months
389
Indications for chest tube insertion
Empyema - pus, positive gram stain, positive culture Very loculated Very septated Massive effusion (>50% of hemithorax) pH <7.2 Intermediate pH but LDH >900
390
Complications of pleural infections
Bronchopleural fistula Pleural calcifications Pleural thickening Empyema necessitans (pus extending into the chest wall, common with TB) Fibrothorax
391
Antibiotic for treatment of parapneumonic effusion
Beta lactam + beta lactamase inhibitor Ceftriaxone/FQ + metronidazole Carbapenems Clindamycin Carbapenem + vanco if HAP Duration 2-6 weeks
392
If needed, when is surgery ideally performed RE: pleural effusion?
Within day 3 Should not be favored over chest tube initially VATS is preferred over medical pleuroscopy and thoracotomy
393
Surgical options
Drainage Debridement (removal of lose debris/dead tissue) Decortication (peel of a thick fibrous layer of pleura)
394
Benefits of intrapleural enzyme therapy
Reduces volume on imaging Reduces LOS Reduces requirement for thoracic surgery
395
Indications for giving a reduced dose of intrapleural lytics
Very hemorrhagic fluid at baseline Disease with hemorrhage risk e.g. RCC with lung mets Anticoagulation that cannot be stopped Note: Anticoagulation increases risk to 10% (overall risk 4%) but half dose did not change risk
396
RFs for enzyme related bleeding
Concurrent administration of anticoagulation Elevated RAPID score Plt count <100,000
397
Sites of pneumomediastinum
Alveolar sacs (most common) Tracheobronchial tree Esophageal Bowel rupture
398
Physical examination findings of pneumomediastinum
Hamman’s crunch (crunching with each heart beat or mediastinal crunch) Subcutaneous emphysema High pitched voice
399
Image findings of esophageal rupture
Pneumomediastinum - air around the mediastinum Widened pneumomediastinum Pneumothorax Pleural effusion Subcutaneous emphysema Air under the diaphragm
400
What are the causes of spontaneous pneumothorax (categories)
Catamenial Primary Secondary
401
Causes of primary pneumothorax
Asthenic body habitus Subpleural blebs Smoking - cigarettes, marijuana, snorting cocaine Diving
402
Causes of secondary pneumothorax
Bullous lung disease LAM PLCH COPD Asthma Bronchiectasis Thoracic endometriosis Ehler Danlos, Marfans
403
RF for tension pneumothorax development
Traumatic pneumothorax Post CPR pneumothorax On NIV or mechanical ventilation Blocked or kinked chest tube Hyperbaric oxygen treatment Underlying lung disease
404
Mechanisms of hypotension in tension pneumothorax
IVC compression → reduced RV preload RV compression → reduced LV preload Increased LV afterload Increased RV afterload
405
Imaging findings in a tension pneumothorax
Visible lung edge Shifting of mediastinum, deviated trachea Splaying of the ribs
406
Adequate size for intervention for a pneumothorax
>/2 cm laterally or apically on CXR If using CT, any size that can safely be accessed with imaging support Note PSP can often monitor regardless of size
407
Borders of the triangle of safety
Lateral edge of pectoralis muscle Lateral edge of latissimus dorsi Fifth intercostal space/nipple line/breast line (base of breast tissue) Base of axilla
408
High risk features in the treatment algorithm of pneumothorax
Underlying lung disease aka Secondary pneumothorax Age >/50, smoking history Bilateral pneumothorax Hemopneumothorax Tension pneumothorax/hemodynamic compromise Significant hypoxemia
409
Indications of applying suction for a pneumothorax
The pneumothorax increases in size despite chest tube insertion Fails to improve after 24-48 hours There is persistent air leak
410
Percentage of pneumothorax that resolves per day
1.25 - 2.2% per day Increased by 4-6X via oxygen
411
Indications for a surgical consultation in pneumothorax
Recurrent pneumothorax, ipsilateral or contralateral First pneumo BUT: - SSP and significant physiological compromise - Tension pneumothorax/hemodynamic compromise - Spontaneous hemothorax - Bilateral pneumothorax - Persistent air leak 5-7 days, or lung fails to re expand - Pregnant - High risk occupation
412
What surgical technique is preferred for pneumothorax
VATS > thoracotomy Can do any: bullectomy, pleurectomy, mechanical pleurodesis, chemical pleurodesis
413
When would you consider non surgical but definitive management, e.g. talc slurry?
Unwilling to do surgery Unable to do surgery This is because surgical options more effective
414
Recurrence rate for pneumothorax
PSP → 33% SPS → 13-39% After first recurrence → 60%, after second recurrence → 80%
415
Causes of persistent air leak
Conditions: Pneumothorax, Barotrauma, Infections, Malignancies Procedures: wedge biopsies, lobectomy, LVRS, trauma
416
Treatment options for persistent air leak
Treat underlying infection Add suction Second chest tube or bigger chest tube Blood patch Chemical pleurodesis Surgical options
417
Recommendations re: activities post pneumothorax
No PFTs x 2-4 weeks No flying until resolved at least x 1 week, but can be longer especially if underlying lung disease (Canadian Association of Thoracic Surgeons recommend 1-3 weeks) No diving ever
418
Management of bronchopleural fistula volume of leak in a vented patient
Reduce Pplat Reduce autoPEEP → increase expiratory time, reduce Vt, permissive hypercapnia
419
Causes of malignant pleural masses
Mesothelioma Metastases Lymphoma Malignant fibrous tumour Askin tumour (same as ewing sarcoma, chest wall tumour and is malignant) Sarcoma Extraskeletal osteosarcoma
420
What type of malignancy is primary effusion lymphoma?
Usually diffuse large b cell lymphoma Usually no associated lymphadenopathy
421
DDX for malignant effusions in patients with HIV
Lymphoma Primary effusion lymphoma Kaposi sarcoma Other cancers
422
Most common causes of pleural metastases
Lung (adeno) Breast Lymphoma GI/GU
423
Where in the pleural do malignancies usually start?
Mets - visceral pleura Meso - parietal pleura
424
Non malignant causes of pleural masses
Solitary fibrous tumour of the pleura Lipoma Mesothelial cyst Pleural endometriosis Pleural plaques, thickening (not really masses)
425
What are the associated paraneoplastic syndromes with solitary tumour of the pleura?
Hypoglycemia, Doege-Potter syndrome (elevated IGF) Hypertrophic pulmonary osteoarthropathy
426
Concerning features of pleural malignancy on imaging
Thickness > 1 cm Circumferential thickening Involvement of the mediastinal pleura Diaphragmatic thickening > 7 Nodular thickening
427
Sensitivity of pleural fluid for malignancy
Overall, 60%, increase by 15% with the second tap (MAM paper says 20%) Adenocarcinoma 80% Breast 70% Small 50% Mesothelioma 30% Squamous cell 20%
428
Definition of non expandable lung in MPE
>/25% of the lung is not opposed to the chest wall Is based on CXR
429
Treatment for MPE
Aspiration has shorter LOS but more need for intervention IPC vs chest tube with talc slurry or poudrage
430
Management of MPE in mesothelioma
Talc poudrage preferred Other options IPC, slurry, PP
431
Benefit of MPE management
Improved dyspnea Improved QOL
432
Agents for pleurodesis
Talc Doxycycline Bleomycin
433
Rate of spontaneous pleurodesis once an IPC is inserted
25%
434
Clinical factors suggest will gain improvement with IPC
Improvement after therapeutic thoracentesis Rapid reaccumulation Prognosis is >1 month Supports to have home care
435
Possible side effects from pleurodesis
Chest pain Fever ARDS
436
Treatment of infected/loculated MPE with IPC inserted
Abx Intrapleural enzymes Intrapleural normal saline Extra chest tube Surgical - VATS, decortication
437
How long after asbestos exposure does mesothelioma occur?
~40 years after exposure
438
3 main subtypes of mesothelioma
Epithelioid Biphasic Sarcomatoid (worst prognosis)
439
Causes of mesothelioma
Asbestos (?dose response) Erionite fibers Thoracic radiation SV40 infection, other viral infections Chronic pleural disease
440
Imaging features are concerning for mesothelioma
Pleural thickening with concerning features (see previous) Presence of asbestos exposure Local invasion - chest wall, mediastinum, diaphragm, ribs Usually unilateral changes, usually right side predominance Spreads along pleura and fissures Starts at parietal pleura
441
Diagnosis of mesothelioma
Image guided biopsy Medical pleuroscopy Surgical pleuroscopy/VATS
442
Management of mesothelioma
Double immunotherapy - ipilimumab + nivolumab (previously was chemo, but studies show immunotherapy better) Debulking surgery if candidate (epithelioid and ECOG 0-1) Both improve survival SMART TRIAL NEGATIVE (For radiating ports after BUT trend to significance so maybe underpowered) remuniration and palliative care
443
Poor prognostic markers in mesothelioma
Histology (Sarcomatoid worst) Stage Age Poor performance status
444
Malignant causes of lymphangitic carcinomatosis
Cervical Colon Stomach Breast Prostate, pancreas Thyroid Lung Mneumonic: certain cancers spread by plugin the lymphatics
445
Diagnosis of lymphangitic carcinomatosis
Biopsy - TBBx or surgical
446
Histological findings of lymphangitic carcinomatosis
Obstruction and distension of lymphatics by tumour cells
447
Treatment of lymphangitic carcinomatosis
Treat underlying cancer Steroids, but no clear data Opioids for symptom control
448
How many segments are there in each lobe of the lung?
RUL: 3 RML: 2 RLL: 5 LUL: 5 LLL: 5 or 4
449
Equations for PPO lobectomy and pneumonectomy
Lobectomy PPO FEV1 = FEV1 x [1 - (resected segments/19)] Pneumonectomy = PPO FEV1 = FEV1 x [1 - fraction of perfusion to resected lung] Using absolute value Both greater than 60→ Low risk 30-60% stair climb or shuttle walk Any < 30% then CPET
450
Examples of important post operative complication predictors
VO2 max FEV1 DLCO In place of CPET can use stair climb or shuttle walk.
451
In post operative planning, what are the cutoffs for SWT and stair climbing? Low technology exercise test.
SWT <400 m Stair climb <22m
452
In post operative planning, what are the cutoffs for VO2 max?
<10 mL/kg/minute (<35%)→ high 10-20 → moderate (35-75%) >20 (>75% predicted) → low
453
Patient factors that increase post op complications from non-pulmonary surgery
Age Smoking ASA class OSA COPD (especially if FEV1 <60%) Pulmonary hypertension Low albumin Obesity is not a risk factor
454
Surgical factors that increase post op complications from non-pulmonary surgery
Aortic > intrathoracic > upper abdominal > abdominal Duration of surgery Emergency surgery General anesthesia (epidural better) Paralytics
455
How can post operative complications be prevented?
Optimize underlying lung disease prior to surgery Smoking cessation (>8 weeks previous surgery) Avoid GA if possible; regional blocks if possible Avoid long acting neuromuscular blockade Shorter surgery (<3 hours) Laparoscopic CPAP if OSA Lung expansion techniques Pain control
456
Physiological changes that occur after a pneumonectomy
FEV1, FVC, lung volumes, DLCO decrease Decrease compliance Increased resistance Dead space can increase or decrease RV EF reduces, LV function does not change No change in blood gasses
457
What normally happens to the post pneumonectomy space?
Fills with air, then with fluid Complete opacification takes 4 months
458
Post pneumonectomy complications
Post pneumonectomy syndrome Post pneumonectomy empyema Bronchopleural fistula Esophagopleural fistula Pulmonary embolism Pneumothorax Hemorrhage Arrhythmias, MI
459
When does post pneumonectomy syndrome occur and what is it?
After 6 months following surgery Almost exclusively after right sided pneumonectomy (it is excessive mediastinal shift/rotation resulting in compression and stretching of the tracheobronchial tree and the esophagus)
460
When does post pneumonectomy pulmonary edema occur?
Within 72 hours Non cardiogenic edema/ARDS More common during right vs left
461
RFs for post pneumonectomy pulmonary edema
Right sided resection Large perioperative fluid load Single lung ventilation High inspired O2 concentrations
462
Inclusion criteria for NSLT?
Age 55-74 Current smoker or quit within the last 15 years Has at least 30 pack year smoking history Experienced centers
463
Exclusion criteria for NSLT?
Lung cancer Hemoptysis Lost >/15 lb in the last 1 year Chest CT in the prior 18 months
464
Key differences between the NLST and NELSON trials
Different proportion of males/females Inclusion criteria Nodule management protocol - diameter vs volume Control comparison - CXR vs nothing Follow up - different # and intervals
465
What are the IHC stains for the different cancers?
Adenocarcinoma: TTF1 (if negative but adeno much worse prognosis) Squamous cell: CK5/6. P63 Small cell: TTF1 but also neuroendocrine markers (chromogranin, CD56, synaptophysin)
466
General features of different lung cancers
Small cell - usually central, small primary, usually arises in airways, early mets Squamous cell - usually central, bulky lesion, may cavitate Adenocarcinoma - usually peripheral
467
RFs for lung cancer
Smoking Exposures - nickel, radon, asbestos, silica, beryllium, pollution Underlying conditions - IPF, scleroderma-ILD, COPD, HIV Radiation exposure
468
Health Canada recommendations in regards to radon
If >200, have to hire professional If 200-600, have 2 years to fix If >600, have to fix within 1 year
469
Clinical manifestations of superior sulcus tumour
SVC syndrome (more common if R) Horner’s syndrome (T1) Brachial plexus injury (C8, T1, T2) Recurrent laryngeal nerve involvement (more common if L) Also called a pancoast tumour
470
Neurological findings in superior sulcus tumour
Miosis, ptosis, anhidrosis Laryngeal nerve dysfunction Ulnar nerve distribution abnormalities/brachial plexus involvement Cerebral edema Also called a pancoast tumour
471
Physical exam findings in SVC syndrome
Confusion 2/2 cerebral edema Facial plethora, Proptosis Facial and neck edema Elevated JVP Collateralization of superficial vessels Cyanosis, hypoxemia
472
Causes of SVC syndrome
Malignancy - lung ca, lymphoma Thrombosis Indwelling intravascular device Post radiation fibrosis Fibrosing mediastinitis External compression from sarcoidosis, thyroid goiter
473
Management of SVC syndrome
Emergency → stent; radiation if not surgical candidate Steroids if already have answer, steroid responsive Anticoagulation if thrombosis Chemotherapy if applicable
474
Paraneoplastic syndromes are associated with lung cancer
Encephalitis LEMS Cushing’s syndrome Hyponatremia Hypercalcemia Hypertrophic pulmonary osteoarthropathy (Triad: digital clubbing, periostitis (new bone growth on the bones), and arthropathy) Rashes - dermatomyositis, acanthosis nigricans, erythema multiforme, pruritus, urticaria
475
Imaging and clinical findings of hypertrophic pulmonary osteoarthropathy
Bone scan - Symmetrical, increased linear uptake along diaphyseal and metaphyseal surfaces of long bones XR - smooth periosteal reaction Triad: digital clubbing, periostitis (new bone growth on the bones), and arthropathy
476
Paraneoplastic syndromes are associated with thymoma
Myasthenia gravis Red cell aplasia Cushing’s syndrome Addison’s disease
477
Mechanisms of hypercalcemia in malignancy
Bone metastases PTHrP Granulomas increasing 1,25 vitamin D Ectopic production of PTH e.g. parathyroid carcinoma
478
Where can lung cancer metastasize to?
Brain Pleura Adrenals Liver Bone Bone marrow
479
Lung cancers that usually cause hemoptysis
Squamous cell carcinoma Carcinoid tumour Kaposi sarcoma
480
Lymph node stations and their borders
Superior mediastinal nodes 1: Highest mediastinal 2R inferior border innominate/brachiocephalic vein). 2L Inferior border aorta on left 3: prevascular adn retrotracheal 4R Upper Border innominate/brachiocephalic. Inferior azygos vein. 4L upper border Aortic arch and inferior Pulmonary artery Aortic nodes 5: subaortic 6 para aortic Inferior mediastinal nodes 7 subcarinal 8 paraesophageal nodes 9 pulmonary ligament nodes Hilar nodes, lobar and subsegmental nodes 10 hilar nodes : 10R azygus 10L Pulmonary Artery 11 Interlobular: 11s between upper lobe bronchus and bronchus intermedius. 11i between the middle and lower lobe bronchi 12 lobar: adjacent to lobar bornchi 13 segmental nodes: adjacent to segmental bronchi 14 sub segmental: adjacent to subsegmental bronchi.
481
Suspicious features of lymph nodes?
Canada Lymph node score: Clear margins Loss of central hilar structure Central necrosis Short axis diameter >/1 cm Also known as Canada Lymph Node Score
482
What stations can be accessed by different methods
483
Molecular markers for adenocarcinoma
EGFR (15% of canadians with adeno) ALK ROS1 PDL-1 BRAF
484
Molecular markers for squamous
PDL-1
485
Who requires brain imaging?(In Lung Ca)
Clinical signs or symptoms concerning for brain metastases Clinical stage II, III or IV non small cell lung cancer Maybe IB but definitely not IA
486
When would you consider staging the mediastinum
- Discrete mediastinal node enlargement, no distant mets - Node SUV >/2.5 - Peripheral tumour BUT:I nner ⅔ of lung (more central); >/3 cm = greater than T1; Associated with enlarged mediastinal LN >1 cm - Central tumour: Radiographically enlarged or PET avid nodes
487
When would you NOT need to do mediastinal staging?
Peripheral T1N0 disease not meeting criteria above Bulky tumour invading mediastinal structure - need tissue, but does not need to be from nodes Metastatic disease - biopsy whatever gives you highest stage
488
Sensitivity and specificity of CT, PET, EBUS, mediastinoscopy for mets
CT: sp 80/sn 55 PET: sp 85/sn 80 EBUS: sp 100/sn 90 (ONLY 55% for LYMPHOMA but sp 100%) Mediastinoscopy: sp/100/sn 80
489
Treatment for SCLC
Limited - Chemo + radiation followed by adjuvant immunotherapy - If good response and normal brain MRI can do prophylactic cranial radiation - If VERY Limited consider surgery Extensive - Chemo + immunotherapy - Immunotherapy adds 2-3 months of survival - Cranial Radiation
490
Indications for cranial radiation in SCLC
1. Prophylaxis - Limited stage, good response to chemo - Extensive stage 2. Evidence of brain mets
491
Benefits of prophylactic cranial rad in SCLC
Limited disease: decrease brain mets, improve survival Extensive disease: decrease brain mets, no change in survival ? (Lancet review 2024 says PCI is associated with survival benefit but when factor in MRI to exclude brain mets then this benefit disappeared suggesting more therapeutic benefit rather than prophylactic)
492
Indications for cranial radiation in NSCLC
Brain mets with no targeted mutations Otherwise, we use targeted therapy and if symptomatic/risk herniation, surgical
493
Treatment for NSCLC
494
Possible side effects of immunotherapy
Cutaneous/rash Uveitis *Pneumonitis Hypothyroidism, hyperthyroidism *Hepatotoxicity *Colitis, diarrhea Pancreatitis *all EGFR -Rash/acne ALK -Cardiac (Bradycardia, HTN)
495
When does checkpoint inhibitor toxicity usually occur?
Median 3 months, can be up to 19 months
496
When should you discontinue checkpoint inhibitor permanently after pneumonitis?
G3 or higher
497
Checkpoint inhibitor lung related toxicity
Immune related pneumonitis Radiation recall pneumonitis
498
Grading of Immune therapy toxicity and treatment.
Grade 1: Asymptomatic with radiographic changes Grade 1: Continue therapy with close observation, escalate to treatment for symptoms or radiographic worsening Grade 2: Symptomatic but no limitation of usual activity Grade 2: Hold therapy, consider bronchoscopy, institute oral prednisone 1 mg/kg/day if no improvement Grade 3: Symptomatic, with oxygen requirement or limitation of activity Grade 3-4: Discontinue therapy, bronchoscopy, institute oral prednisone 1-2 mg/kg/day or IV corticosteroids at equivalent dose Grade 4: Severe or life-threatening
499
Side effects of tyrosine kinase inhibitors (ex. dasatinib)
Cutaneous, rash Ocular toxicity Pulmonary - pneumonitis Colitis, diarrhea Hepatic toxicity
500
Side effects that should lead to permanent discontinuation of tyrosine kinase inhibitors
Confirmed ILD as a result Ulcerative keratitis GI perforation SJS, severe skin disease
501
Treatments for bony met pain
Opioids, NSAIDs Bisphosphonates, denosumab - osteoclast inhibitors Radiation Steroids Regional anesthesia
502
Pathological types of adenocarcinoma spectrum of disease
1. Atypical adenomatous hyperplasia 2. Adenocarcinoma in situ (<3cm and formerly BAC) 3. Minimally invasive adenocarcinoma (<3cm lepidic predominant with <5mm invasion) 4. Invasive adenocarcinoma (>5mm) - Lepidic - Acinar - Micropapillary - Papillary - Solid predominant 5. Variants of invasive - Invasive mucinous - Colloid - Fetal
503
Radiographic abnormalities for adenocarcinoma spectrum
Solid nodule GGO nodule, subsolid nodule Mass Multiple pulmonary nodules Patchy consolidation, lobar consolidation Crazy paving
504
Differences between typical and atypical NETS
DIPNECH = preinvasive - <5 mm Typical = > 5 mm, <2 mitoses/10 HPF, no necrosis Atypical: 2-10 mitosis or necrosis SCLC: >11/10 mitoses HPF
505
Clinical manifestations of carcinoid tumors
Dyspnea, wheeze Hemoptysis Carcinoid syndrome - flushing ,telangiectasias, diarrhea Cushing syndrome Acromegaly syndrome
506
Investigation options in carcinoid tumors
Serum chromogranin A 5-HIAA Somatostatin receptor based imaging e.g. OctreoScan, Gallium PET - low grade/typical only weakly positive
507
Bronchoscopy features of carcinoid tumour
Mainly proximal airways Well vascularized
508
RFs for malignant nodules
Number - increased 1-4, decreases >/5 Size Doubling time 20-400 days Enhancement Appearance - subsolid, spiculated, lobular, Carona Radiata (LR 14) Calcification pattern Location - upper lobe Evidence of emphysema Smoking history
509
Usually benign patterns of calcification
Diffuse Central Lamellar Popcorn
510
Causes of a negative PET scan
Less metabolically active tumors Solid component <8 mm Uncontrolled hyperglycemia
511
Who do the Fleischner Society Guidelines apply to?
>/35 years old Not immunocompromised No history of cancer Not for cancer diagnosis (applies to incidentally found nodules) No symptoms attributable to lesion
512
Low vs high risk by the Fleischner Guidelines
Low: minimal or absent smoking hx or other RF High: hx of smoking or other known RF (e.g. fhx first degree, asbestos/radon/uranium exposure)
513
How long do pulmonary nodules need to be followed?
Solid nodules - 2 years Subsolid nodules >/5 years
514
DDX for benign pulmonary nodules
Infectious nodules Inflammatory, vasculitic Vascular (AVM) Hamartoma Hemangioma Fibroma Lipoma Leiomyoma Amyloidoma
515
Radiographic features of a hamartoma
Popcorn calcification Heterogeneous attenuation Rounded or lobular borders
516
Difference between teratoma and hamartoma
Teratoma occur in anterior mediastinum Teratoma also include teeth and bone Teratomas may become malignant
517
Draw out the TNM 8th edition and 9th edition.
518
Draw out the Fleishner Society Nodule Chart.
519
Sources of asbestos exposure
Pipefitter Plumbers Motor vehicle mechanic Construction worker Shipyard worker
520
Different types of asbestos fibers
Serpentine (long) and amphibole (short) are the two general types 1. Serpentine * Chrysotile (most common) 2. Amphibole * Actinolite * Anthophylllite * Amosite * Tremolite * Crocidolite (Most dangerous/highest risk of mesothelioma)
521
RFs for developing asbestosis
Exposure at a young age Duration and extent of exposure Amphibole > chrysotile Concomitant smoking
522
Pulmonary manifestations of asbestos
Rounded atelectasis Asbestosis Pleural plaques Pleural thickening Benign asbestos related pleural effusion Mesothelioma
523
Imaging findings of asbestosis
Lower lobe distribution Reticular changes Rounded atelectasis Pleural plaques Honeycombing and interlobular septal thickening Lower lobe distribution Reticular changes
524
Pathological findings of asbestosis - How is it different from UIP?
2 or more asbestos bodies per square centimeter of a 5-mu thick lung section in combination with interstitial fibrosis are indicative of asbestosis Asbestos has presence of asbestos bodies Has mild fibrosis of the visceral pleura Fibroblastic foci are infrequent
525
How do you diagnose asbestosis?
ATS 2004 need 3/3 2. 1. Evidence of structural change as demonstrated by one or more * Imaging * Histology 1. Evidence of exposure/cause * occupational/environmental history with latency * Markers of exposure (pleural plaques) * Asbestos bodies 1. Exclusion of other diagnosis
526
What is the treatment of asbestosis?
Supportive care: * Steroids pred 0.5-1mg/kg for 1-3 months then taper for 1-3 months and steroid sparing agents can be used but unclear benefit. * Smoking cessation and co-existing airways disease treatment * Immunizations * Oxygen * decortication * Lung transplant
527
Where do pleural plaques usually occur?
Bases (posterolateral) and mediastinal pleura Can also involve the diaphragm Spares apices and costophrenic angles May be calcified but most are not
528
What is the CT definition of pleural thickening?
In general >3 mm thick
529
Fluid features of BAPE
Exudative Eosinophilic usually Can be bloody Usually spontaneously resolves, can recur
530
Occupations with beryllium exposure
Electronics Nuclear industry, nuclear weapons Aerospace industry Fluorescent light bulbs Beryllium mining Ceramics
531
Routes of sensitization for beryllium
Inhalation Skin
532
Pulmonary manifestations of berylliosis
Acute pneumonitis Chronic beryllium disease
533
Non pulmonary manifestations of berylliosis
Conjunctivitis (no uveitis, or retinal involvement unlike sarcoid) Periorbital edema Nasopharyngitis Tracheobronchitis
534
Imaging findings of berylliosis
Acute pneumonitis: ARDS, non-cardiogenic pulm edema Chronic beryllium disease: sarcoid but LN less likely
535
Biopsy findings of CBD (chronic berylliosis disease)
Typically on TBBx Granulomas Distribution paraseptal, interlobular septa, peribronchovascular
536
Diagnostic criteria of CBD (chronic berylliosis disease)
Positive BeLPT (blood or BAL) (Beryllium lymphocyte proliferation test) Non caseating granuloma and/or mononuclear cells on biopsy Clinical dx if no bx: BAL lymphocytosis or imaging
537
Definition of positive BeLT (Beryllium lymphocyte proliferation test)
1 BAL BeLPT 2 blood BeLPT Positive skin patch sensitization test (DON’T do because can lead to sensitization in beryllium naive individuals) +2 Simulation Indices =abnormal BeLPT , + 1 Simulation Indices =borderline
538
Difference between beryllium sensitization and Chronic Berylliosis disease)
Sensitization: sensitization, no sx, normal biopsy Subclinical: sensitization, + biopsy, no sx/rads CBD: sensitization, + biopsy, +sx/rads
539
Treatment of CBD
Observe Steroids if symptoms or PFT change with consideration for steroid sparing agents if not tolerated
540
Pulmonary manifestations of silicosis
Acute silicoproteinosis Accelerated proteinosis Chronic, simple silicosis Complicated silicosis, progressive massive fibrosis
541
Complications of silicosis
Tuberculosis, NTM Lung cancer CTD/Erasmus syndrome (Systemic Sclerosis) PAP Fibrosing mediastinitis
542
Radiographic manifestations of silicosis
Crazy paving Perilymphatic nodules and upper lobe Mediastinal and hilar LN, eggshell calcification Progressive massive fibrosis Hyperinflation, COPD Cavitary lung disease Ground glass nodules/opacities
543
Diagnosis of silicosis
Exposure history Imaging findings BAL if silicoproteinosis Biopsy avoided due to PNTX risk
544
Treatment of silicosis
Acute → steroids Chronic → supportive
545
Pulmonary manifestations of CWP
Simple chronic CWP Complicated CWP, progressive massive fibrosis Caplan syndrome (rheumatoid pneumoconiosis) Not associated with lung cancer unlike others
546
Imaging findings of CWP
Crazy paving Perilymphatic nodules Mediastinal and hilar LN, eggshell calcification Progressive massive fibrosis Hyperinflation, COPD Cavitary lung disease (eggshell less common ) Similar as above, but eggshell less common Typically diffuse perilymphatic small nodules 30% have hilar/mediastinal lymph node enlargement but calcification less likely
547
Examples of hard metal lung disease
Cobalt related lung disease Siderosis (iron dust) Metal fume fever (zinc fumes)
548
Lung diseases that are associated with cobalt exposure
Occupational asthma Interstitial lung disease - giant cell interstitial pneumonia Obliterative bronchiolitis
549
Inorganic and organic inhalational causes of pneumoconiosis
Inorganic: coal, silica, beryllium, asbestos Organic: cotton, tobacco, sugarcane, basically anything can cause HP
550
Pulmonary manifestations of byssinosis
Airway obstruction Uniquely worse on the first day of work and then improves Typically with raw cotton exposure
551
Causative agent of Silo Filler’s disease
Silo gas = combination of nitrogen dioxide and carbon dioxide Nitrogen dioxide + water in lungs → nitric acid
552
Pulmonary manifestations of silo filler’s disease
ARDS Obliterative bronchiolitis
553
Exposures associated with lung cancer development.
Uranium mining Beryllium Asbestos Silica
554
Causes of PMF?
Sarcoidosis Berylliosis Silicosis CWP Talcosis
555
CTD causes of UIP
RA SSc SLE DM/PM
556
Extraparenchymal findings on CT that suggest CTD-ILD
Esophageal dilatation Pleural or pericardial effusion Lymphadenopathy C1-2 subluxation
557
RFs for development of RA-ILD
Male Older Smoking RF positive Anti-CCP positive Disease activity MUC5B
558
RFs for RA pulmonary nodules
Subcutaneous nodules Longstanding RA
559
RFs for RA pleural effusion
Male Older age Rheumatoid nodules
560
Pulmonary manifestations of RA
RA-ILD - UIP, NSIP, LIP, OA, CPFE Diffuse alveolar hemorrhage RA pulmonary nodules Caplan syndrome Pulmonary hypertension Pleural effusion Pneumothorax Follicular or obliterative bronchiolitis Bronchiectasis Cricoarytenoid arthritis Vasculitis of vocal cords RA nodules on vocal cords
561
Imaging features of RA related lung disease
Nodules Cavities Pleural effusions Pneumothorax Bronchiectasis UIP pattern or others Findings of PH e.g. edema, enlarged heart, etc.
562
BAL cell count and differential in RA-ILD
Lymphocytic in NSIP Neutrophilic in UIP
563
Treatment of RA related lung disease
RA-ILD: steroids, MMF, cyclophosphamide, antifibrotics Bronchiectasis: same as others Bronchiolitis: treat RA, consider azithromycin
564
What are pulmonary manifestations of scleroderma?
ILD - NSIP, UIP, OP, PPFE Pulmonary hypertension, PVOD Airway disease - follicular/obliterative bronchiolitis, bronchiectasis Aspiration pneumonitis or pneumonia Lung cancer Chest wall restriction
565
Features associated with early development of SSc-ILD
African american Extensive disease Scl-70 positive CK elevated Cardiac involvement Hypothyroidism
566
eatures associated with SSc-ILD progression
Extent - >20% of lung involved FVC <70% predicted Within 4 years of diagnosis Anti scl-70 Diffuse cutaneous disease
567
Treatment of SSc-ILD
Mycophenolate Cyclophosphamide Tocilizumab Rituximab Nintedanib Nintedanib + mycophenolate
568
Benefits and evidence of SSc-ILD management options
Improve FVC, DLCO → Mycophenolate and cyclo Reduce decline in FVC → ritux, toci, nintedanib Nothing has mortality benefit
569
How often should patients with SSc-ILd be followed?
6 months x 5 years Annually after 5 years (if they were stable
570
Pulmonary manifestations of myositis
ILD - NSIP, UIP, OP, DAD Respiratory muscle weakness Aspiration pneumonia Pneumothorax Pulmonary hypertension
571
Antisynthetase syndrome diagnosis
1. 2 of: - Fever - Raynaud - Mechanics hands/hiker’s feet - Polymyositis - Non-erosive arthritis - ILD 2. Positive autoantibody (Anti-Jo-1)
572
Treatment options for myositis-ILD
Cyclo if very sick MMF, azathioprine
573
Pulmonary manifestations of lupus
Interstitial lung disease - NSIP, UIP, LIP Acute pneumonitis (similar to AIP) Organizing pneumonia DAH Pleural effusion * most common Shrinking lung syndrome VTE Pulmonary hypertension - PVOD, PAH, Group 2,3,4 Subglottic stenosis, tracheal stenosis Bronchiolitis obliterans Opportunistic infections
574
Skin manifestations of lupus
Acute cutaneous lupus erythema Panniculitis Discoid lesion Childpain lupus erythematosus (pernio)
575
Pulmonary manifestations of Sjogren’s syndrome
Interstitial lung disease - e.g. NSIP, LIP, UIP Organizing pneumonia Bronchiolitis - follicular, obliterative Bronchiectasis Xerotrachea Aspiration pneumonitis and pneumonia Pulmonary hypertension Nodular hyperplasia Pulmonary nodular amyloidosis Pulmonary lymphoma (transformation)
576
Pulmonary manifestations of amyloidosis
Nodular pulmonary amyloidosis Diffuse amyloidosis Tracheobronchial amyloidosis Amyloidosis of the pleura
577
Clinical Features of patients with CTD-ILD (SARD-ILD) Epidimiology by Condition
578
ACR 2023 Screening guidelines for SARD-ILD
579
How to screen people with SARD of interest?
580
What are the first line therapies by disease type of CTD ILD according to ACR 2023?
581
Management of Rapidly progressive ILD.
582
Skin manifestations that may be seen in vasculitis
Palpable purpura Leukocytoclastic vasculitis Lacrimal gland inflammation Skin ulcerations ?saddle nose deformity ?stawberry gums (gingivitis)
583
Differential diagnosis for ANCA elevation
Vasculitis CTD Malignancies Infections - hepatitis B/C/HIV Drug induced (PTU, methimazole, hydralazine, allopurinol) IBD
584
% of ANCA elevation in different conditions
GPA - 90% c anca/ PR3 MPA - 70% p anca/mpo EGPA - 50% p anca/mpo Anti-GBM - 10%
585
Classic triad of DAH
Hemoptysis Anemia Alveolar opacities
586
DDX of DAH
1.Vasculitis - GPA - EGPA - MPA - Drug induced vasculitis 2. Connective tissue diseases - SLE - Anti-GBM - Rheumatoid arthritis - Scleroderma - Others 3. Drugs - TNF-alpha inhibitors - Hydralazine - Anticoagulation - GPIIb/IIIa platelet inhibitors - Amiodarone - Crack cocaine 4. Others - IPH Idiopathic pulmonary hemosiderosis - Left sided pressure increase e.g. mitral stenosis - HHT hereditary hemorrhagic telangiectasias
587
BAL findings of DAH
Hemosiderin laden macrophages >/20% Progressively bloody sequential lavage
588
ANCA + vasculitis that cause DAH
GPA MPA EGPA (very rarely) Drug induced ANCA vasculitis Isolated pulmonary capillaritis Anti-GBM/ANCA positive vasculitis
589
DDX for pulmonary renal disease
Anti-GBM GPA, MPA, EGPA ANCA negative vasculitis e.g. cryo, IgA disease SLE
590
RFs for GBM development
Smoking Cocaine use Hydrocarbon fume exposure Hair dye exposure Metallic dust Genetics
591
Sensitivity and specificity of anti-GBM
Sensitivity 95-100% Specificity 90-100%
592
Causes of false positive anti-GBM
Hepatitis C HIV
593
Poor prognostic factors in anti-GBM
Advanced age Anti-GBM titre Renal function - crea & need for dialysis at presentation, oligoanuric, % crescents (only pathological parameter)
594
Treatment of anti-GBM
Steroids, cyclophosphamide PLEX No maintenance Abx if pulmonary involvement
595
Role of anti-GBM in disease monitoring
Monitor regularly (Weekly for 6 weeks and should be undetectable x2 occasions then q2weekly x2, then monthly x 6 months Should disappear with treatment May signal recurrence (re-treat)
596
Pulmonary manifestations of GPA
Wedge shaped opacities due to infarction Nodules Cavities Interstitial lung disease - NSIP, UIP Diffuse alveolar hemorrhage Subglottic or tracheal stenosis Tracheobronchomalacia
597
Extrapulmonary manifestations of GPA
Cutaneous - palpable purpura, leukocytoclastic vasculitis ENT - hearing loss, sinusitis, nasal septal perforation, saddle nose, nasal ulcers Renal - GN, renal failure Systemic symptoms
598
Diagnostic criteria of GPA
599
What is the treatment for GPA?
600
What is considered a severe vs non severe GPA?
Severe = organ threatening disease E.g. RPGN, DAH, mononeuritis multiplex, optic neuritis
601
What are indications to use cyclophosphamide over rituximab in induction treatment?
RPGN with crea >354 if not available
602
What are indications in which PLEX Is needed in GPA/MPA?
RPGN crea >500, need for dialysis (KDIGO) DAH salvage therapy Double positive (with Anti-GBM)
603
Indications in which PLEX is indicated for DAH
Anti-GBM disease Anti-GBM/ANCA double positivity DAH salvage therapy, critically unwell TTP related DAH Catastrophic APLS DAH
604
PEXIVAS trial re: PLEX in ANCA vasculitis
No mortality benefit No impact on ESRD (trend towards improving ESRD progression in high risk patients) Increased risk of infection
605
General differences between MPA and GPA
p-ANCA (in MPA) Mainly renal, less ENT, less pulmonary (in MPA) Absence of granuloma formation (In MPA)
606
What is the diagnostic criteria for MPA
607
What vasculitis is associated with PA aneurysms?
Behcet’s disease (vasculitis with mouth ulcers, swollen joints and eye inflammation) Hugh Stovin syndrome (large vessel similar to Behcet’s) M 20-40 with dvt and bronchial aneurysms. Pulmonary hypertension Congenital heart disease Syphilis Tuberculosis Behcet’s disease Hugh Stovin syndrome Congenital heart disease Syphilis Tuberculosis
608
DDX of pulmonary angiitis and granulomatosis
Bronchocentric granulomatosis Lymphomatoid granulomatosis Necrotizing sarcoid granulomatosis GPA, EGPA
609
Non-pulmonary clinical manifestations of EGPA
Asthma /obstructive airways disease Peripheral nerve (mononeuritis multiplex) Skin disease (purpura, sub cutaneous nodules, urticaria, leukocytoclastic vasculitis) ENT (Nasal polyps), cardiac: effusions, dilated CM, GI, renal
610
What is the diagnostic criteria for EGPA
611
What is the management of EGPA
612
Five factor score
Age >65 Cardiac insufficiency Renal insufficiency GI involvement Absence of ENT symptoms For prognosis and higher score associated with higher mortality
613
Monitoring in management of EGPA and GPA
EGPA - ESR and eos count TTE (Don’t stop leukotriene receptor antagonists) GPA - not ANCA
614
What is the KDIGO 2024 treatment algorithm for Anca Associated Vasculitis
615
Non-infectious complications of illicit drug use
Eosinophilic pneumonia Hypersensitivity pneumonitis Organizing pneumonitis Obliterative bronchiolitis Pneumothorax Pneumomediastinum Drug induced ANCA vasculitis, DAH Pulmonary hypertension Alveolar hypoventilation Aspiration Foreign body granulomatosis Non cardiogenic pulmonary edema E-VALI
616
Complications associated with vaping
Lipoid pneumonia* Eosinophilic pneumonia Organizing pneumonia Hypersensitivity pneumonitis AIP, ARDS VALI
617
Causative agent of vaping induced injury
Vitamin E acetate in e-liquids
618
Diagnostic criteria for EVALI
E cigarette use in 90 days before symptoms Pulmonary infiltrates Negative viral panel, negative cultures, negative other workup
619
IST that are not teratogenic
Azathioprine (purine synthesis inhibitor) Hydroxychloroquine (antimalarial) Cyclosporine, tacrolimus (Calcineurin inhibitors)
620
Patterns of drug induced lung disease
1. Most common: Pulmonary edema (usually w/o effusion) Pulmonary hemorrhage DAD OP, NSIP, UIP EoPNA 2. Less common: HP Sarcoid like rxn LIP, DIP Constrictive bronchiolitis -predominantly penicillamine PHTN, vasculitis
621
Risk factors for MTX induced lung toxicity
Age >60 Underlying pleuroparenchymal lung disease Low albumin Reduced kidney function Third spacing e.g. pleural effusion Higher weekly doses Previous use of DMARDS Diabetes
622
Pulmonary manifestations of MTX toxicity
Hypersensitivity pneumonitis* NSIP AIP with non cardiogenic edema* Eosinophilic pneumonia Organizing pneumonia* Diffuse alveolar damage Pleural effusion* Lymphadenopathy Infections e.g. PJP
623
Extrapulmonary manifestations of MTX toxicity
Transaminitis Stomatitis, nausea/vomiting Mouth sores Macrocytosis, myelosuppression (Increased risk of lymphoproliferative disorders) nephrotoxicity
624
Diagnostic criteria for MTX toxicity
1.Major criteria HP by histopathology without evidence of infection Imaging findings (diffuse pulmonary ground glass or consolidative opacities) Negative blood culture and sputum culture 2. Minor criteria Dyspnea <8 weeks Non productive cough SpO2
625
Differentiate between RA-ILD and MTX toxicity
Clinical presentation - toxicity more subacute/acute Blood work - Eos in toxicity Imaging - NSIP/HP in toxicity, UIP in RA-ILD BAL - both can have lymphocytes Biopsy - NSIP/HP/others in toxicity, UIP in RA-ILD
626
Causes of drug induced lupus
Procainamide Isoniazid TNF-alpha inhibitors Hydralazine
627
Normal pulmonary pressures
sPAP: 15-30 dPAP: 4-12 mPAP: 8-20
628
Hemodynamic diagnosis for pre capillary PH
mPAP > 20 PVR > 2 PCWP
629
Indications to screen for pulmonary hypertension
Scleroderma - annual with DLCO and TTE (ERS DETECT algorithm, CTS position statement on PH) Portal hypertension, prior to transplantation
630
Causes of Group 1 PH
631
Causes of group 2 PH
632
Causes of Group 3 PH
633
Mechanisms of PH in COPD
634
Causes of Group 4 PH
635
What are hereditary causes of PH
BMPR2 (Most Common) EIF2AK4 ALK-1 SMAD9
636
Infectious causes of pulmonary hypertension
Schistosomiasis HIV Hepatitis B/C → cirrhosis
637
Drugs are associated with the development of PH
Toxic rapeseed oil Amphetamines Dasatinib Fenfluramine St John’s Wort Cocaine Cyclophosphamide (alkylating agents)
638
Features make PH-LHD likely
Age >70 Atrial fibrillation Diabetes, DLP, HTN, Obesity (>2 factors) LBBB or LVH on ECG LA dilation, LVH, or grade >2 mitral flow on echo
639
Valvular diseases are most implicated in PH
Mitral stenosis** Aortic stenosis* Mitral regurgitation
640
Causes of PA obstruction
CTEPH Foreign body emboli Schistosomiasis/parasitic infection Vasculitis PA sarcoma, uterine sarcoma, germ cell tumors, RCC Congenital stenosis, other causes of stenosis Obstruction by lymph nodes
641
Causes of group 5 PHTN
Polycythemia vera Essential thrombocytosis Paroxysmal nocturnal hemoglobinuria CML Sickle cell anemia Thalassemia Hereditary spherocytosis Fibrosing mediastinitis Sarcoidosis PLCH Neurofibromatosis Gaucher’s disease CKD with or without dialysis Pulmonary tumour thrombotic microangiopathy
642
Pathogenesis of PAH
Altered tone → vasoconstriction Smooth muscle medial hypertrophy Neointimal formation/hyperplasia and fibrosis Microthrombi/n situ thrombosis causing plexiform lesions
643
Mechanisms for sarcoidosis related PH
Interstitial lung disease Cardiomyopathy Granulomatous inflammation and involvement of vessels → intrinsic sarcoid vasculopathy PVOD lesions Lymph node compression of PA CTEPH Portal hypotension Fibrosing mediastinitis
644
Mediators of portopulmonary hypertension
Estrogen Endothelin 1 Deficiency of prostacyclin
645
Physical examination findings of PH
Loud P2 RV heave Tricuspid or pulmonary regurgitation murmurs Elevated JVP, peripheral edema, ascites
646
Features associated with poor prognosis in PAH
NYHA IV ** Syncope Rapid symptom progression pro-BNP >1100 ng/L or BNP > 800 ng/L ** 6MWD <165 m ** RA size >26 cm^2 Pericardial effusion VO2 max <11 mL/kg/minute VE/VCO2 >45 CI <2, SvO2 <60%
647
Poor RHC prognostic factors
CI <2 RAP >14 SvO2 <60% Vasoreactivity
648
Echocardiographic features of PH
TRV >2.8 m/s RVSP 35 - 40 mmHg RV hypertrophy, RV and RA dilation Flattening of the interventricular septum (can also get bowing) Pericardial effusion Tricuspid regurgitation TAPSE <18 mm IVC >21 mm, <50% collapse with sniff testing
649
Additional echo signs as per the ERS guidelines
Ventricle: RV/LV basal diameter >1, flattening of septum PA: RV outflow doppler acceleration time <105 ms, PA diameter >/25 mm IVC and RA: diameter >21 mm with <50% collapse with deep inspiration, RA >18 cm^2
650
ECG findings of PH
RV strain pattern - most sensitive Right axis deviation RBBB RV hypertrophy - R/S >1 in V1 RA enlargement - P pulmonale, P wave >0.25 mV in lead II
651
CXR findings in PH
Vascular pruning Enlarged pulmonary arteries Enlarged heart - enlarged RV and RA
652
CT findings in PH
Mosaic attenuation Enlarged PA >3 cm PA: aorta ratio > 1 RV increased thickness, interventricular septum changes
653
Ways of measuring CO in PH
Direct Fick method Indirect Fick method Thermodilution method
654
Indications for iron replacement in PH therapy
Ferritin <100 Ferritin 100-299 but tSAT <20%
655
Indications for prophylactic anticoagulation in PH
Idiopathic Hereditary Drug and toxin induced (related to anorexigens) It is “suggested” and warfarin is the agent NOTE: This is 2015 recommendation. 2022 says not generally recommended but consider individually
656
Agents used in vasodilator testing
Inhaled nitric oxide IV epoprostenol IV adenosine
657
Positive vasodilator response in PH
>10 mmHg reduction to
658
MOA of PH medications
Prostacyclin → activates cAMP → inhibits platelet activation, promotes vasodilation Selexipag is prostacyclin receptor agonist Nitric oxide: PDE5i reduce breakdown of cGMP, riociguat stimulates guanylate cyclase which increases production of cGMP. cGMP Endothelin receptor antagonist → inhibition → vasodilation
659
Side effects associated with PH medications
Prostacyclin - hypotension, flushing, headaches, jaw pain, rebound PH PDEf5 - headaches, flushing, volume overload, priapism Riociguat - headaches, headache, GERD ERA - fluid retention, hepatotoxicity, anemia
660
Contraindications to PH therapies
Teratogenic: ERAs, riociguat Heart failure: prostacyclins
661
Combination of which drugs have RCT level of evidence in PH
Tadalafil + ambrisentan AMBITION trial
662
Treatment of PH, what are considered cardiopulmonary comorbidities?
Conditions associated with left ventricular diastolic dysfunction. 1. Cardiac Obesity Hypertension Diabetes CAD 2. Pulmonary Parenchymal disease (DLCO usually <45%) Treatment of refractory PH
663
Treatment of refractory PH
Transplantation Right to left shunt creation
664
Tests for PH need to be done at EVERY follow up
WHO FC 6MWD BNP ECG ABG or pulse oximetry
665
Clinical classification of PAH associated with CHD and their treatment
Small/coincidental defects (<1 c, VSD, <2 cm ASD) → defect closure is C/I Prevalent systemic to pulmonary shunt → may be correctable or non correctable Eisenmenger Syndrome → defect closure is C/I PAH persisting post defect correction
666
In lung disease, what factors actually favor group 1?
Moderate to severe PH rather than mild-moderate FEV1 >60% in COPD FVC >70% in IPF Low diffusion capacity out of keeping CT abnormalities only modest
667
What differentiates non severe from severe group 3 PH?
PVR >5 This is also prognostic indicator
668
Percentage of patients with acute PE develop CTEPH
3%
669
Risk factors for CTEPH
Large burden of disease Recurrent PEs Insufficiency anticoagulation Hypercoagulable states e.g. splenectomy, antiphospholipid syndrome, ET/PCV, malignancy
670
Sensitivity and specificity of imaging in CTEPH
VQ scan >97% sensitive, 90% specific CT PA 99% specific, 51% sensitive
671
CT findings in CTEPH
Webs and Slits Ring like stenosis Total occlusions
672
Conditions that mimic CTEPH on Imaging
Pulmonary artery sarcoma Fibrosing mediastinitis Sarcoidosis Large vessel vasculitis including takayasu Peripheral pulmonary artery stenosis Congenital pulmonary artery abnormalities In situ pulmonary artery thrombosis Pulmonary Veno Oclusive Disease Moyamoya disease
673
Treatment options for CTEPH
Blood thinners for all (lifelong) Pulmonary artery endarterectomy Balloon pulmonary angioplasty Riociguat
674
Possible post endarterectomy complications
Reperfusion injury
675
Possible post Balloon Pump Angioplasty complications
Dissection Perforation Over dilation
676
Imaging findings in PVOD
Smooth interlobular septal thickening Centrilobular nodules Mediastinal lymphadenopathy
677
Etiologies that have been associated with PVOD
Hereditary - BMPR2, EIF2AK4 Medications e.g. cyclophosphamide, bleomycin CTD e.g. scleroderma, SLE, sjogren’s, etc. Infections e.g. influenza, HIV, EBV, CMV HSCT
678
Clinical features that differentiate PCH from PVOD
Hemoptysis Hemorrhagic pleural effusions
679
Histological features of PVOD
Obliteration/extensive and diffuse occlusions of pulmonary veins Colander like lesions (recanalized thrombus) No plexiform lesions
680
Reasons for immediate refferal to PH Centre
1. Warning signs : * 1. rapid progression of symptoms * 1. severely reduced exercise capacity * 1. pre-syncope or syncope on mild exertion * 1. signs of right heart failure. 1. PAH suspected 1. CTEPH suspected
681
Diagnostic Algorithm for PH
682
Components of the 3 strata model
683
Components of the 4 strata Model
684
Treatment algorithm for PAH
685
Definition of platypnea and orthodeoxia
Platypnea = dyspnea in upright position that improves when supine Orthodeoxia = SaO2 drops by >/5% and PaO2 drop by 4 mmHgwhen rising from supine to upright
686
Causes of orthodeoxia
Hepatopulmonary syndrome PAVMs Intracardiac shunts e.g. PFO Pulmonary parenchymal disorders Other causes of VQ mismatch
687
Mechanisms of hypoxemia in HPS
V/Q mismatch - Intrapulmonary vascular dilatations Shunt - Pulmonary arteriovenous malformations Diffusion limitation - due to increased diameter from dilatation
688
Triad of HPS/What is the diagnostic criteria?
Liver disease Intrapulmonary vascular dilatation Abnormal oxygenation (abnormal A-a gradient or PaO2)
689
Treatment options for HPS
Supplemental oxygen Liver transplantation
690
Causes of PAVMs
Idiopathic HHT (>80% of AVM's are from this) Hepatopulmonary syndrome Trauma, prior cardiac surgery Malignant e.g. metastatic thyroid Infections e.g. TB, schistosomiasis CTD e.g. behcet’s, GPA, takayasu
691
Manifestations of PAVMs
Brain abscess Embolic stroke Platypnea, orthodeoxia Hemoptysis, hemothorax Dyspnea (orthodeoxia), Hypoxemia, cyanosis Pulmonary hypertension
692
Additional manifestations of Hereditary Hemorrhagic Telangiectasia (HHT)
PAVM 30% Epistaxis - 90% Telangiectasias - 80% Cerebral AVMs - 10% Hepatic AVMs → high output heart failure GI bleeding, iron deficiency
693
Manifestations of a liver AVM
Portal hypertension Encephalopathy and other signs of liver dysfunction High output heart failure
694
Physical examination findings in HHT
Mucosal and skin telangiectasias Pulsatile liver Murmurs and bruits Platypnea and orthodeoxia Cyanosis and clubbing Signs of heart failure e.g. peripheral edema
695
Investigations to diagnose shunt or PAVMs
O2 saturation on room air Contrast echo/bubble echo 100% oxygen Radiolabeled perfusion scan
696
Investigations to assess the PAVM
CT PA Pulmonary angiography
697
Treatment options for PAVMs
Observation, repeat CT q3-5 years Embolization/embolotherapy Surgical resection Laser ablation
698
Indications for PAVM treatment
Symptomatic, complications, regardless of size Feeding vessel > 3 mm Progressive enlargement
699
Genetics of HHT
Autosomal dominant ACVRL1, ENG, SMAD4
700
Diagnostic criteria for HHT
Curacao Criteria - Mutation OR (3 for definite, 2 for suspected) - First degree relative with HHT - Multiple mucocutaneous telangiectasias - Visceral involvement of telangiectasias or AVMs - History of recurrent and spontaneous epistaxis
701
Screening for in patients with HHT
Iron deficiency anemia* Pulmonary AVMs* Cerebral AVMs* GI AVMs Hepatic AVMs
702
Diagnostic criteria for amniotic fluid embolism
During labor/delivery or within 30 mins of placenta delivery [Cardiopulmonary collapse or sBP <90] AND resp compromise (hypoxemia, dyspnea, cyanosis) DIC Absence of fever
703
Diagnostic criteria for fat embolism
Petechiae Neurological symptoms e.g. coma, seizure Hypoxemia
704
Causes of fat embolism
Fractures, orthopedic surgeries Liposuction, lipoinjection Panniculitis Burns Pancreatitis Fatty liver disease Sickle cell disease Osteonecrosis
705
Treatment of amniotic fluid embolism, fat embolism, Venous air or arterial air embolism
Amniotic fluid - supportive Fat embolism - supportive, ?steroids controversial Venous air embolism - left lateral decubitus (durant Mavouver), hyperbaric O2 Arterial air embolism - hyperbaric O2
706
Indications for bilateral lung transplantation
CF/bronchiectasis/suppurative lung disease Pulmonary hypertension
707
Contraindications to single lung transplant in IPF
Colonization with resistant organisms, bronchiectasis Pulmonary hypertension
708
Overall survival post lung transplant
Overall mean 6.5 years Double lung transplant mean 8 years Single lung transplant mean 5 years
709
Associated side effects with CNIs
Neuro - tremors, headaches, visual abnormalities, seizures Cardiovascular - hypertension Renal - AKI, hyperkalemia, hyperuricemia, gout MSK - osteoporosis Endo - hirsutism, hyperglycemia Drug drug interactions 1. 1. CYP3A4 enzyme inhibitors * 1. increases calcineurin inhibitor levels * 1. Macrolides (except azithromycin), Azoles, Calcium channel blockers, Grapefruit juice 1. CYP3A4 enzyme inducers * 1. Decreases calcineurin inhibitor levels * 1. Rifampin, Carbamazepine, pheobarbital, pheytoin * 1. St. John’s wort
710
Classes of Immunosuppresion in transplant
711
General SE for Lung Transplant immunosuppressive medications
712
Required prophylaxis post lung transplant
PjP prophylaxis for all CMV prophylaxis for those at risk HSV for all EBV for those at risk Aspergillus for those at risk
713
General Lung Transplant Criteria
Chronic end stage lung disease who meet both criteria * >50% risk of death from lung disease within 2 years if lung transplant not performed * >80% likelihood of 5-year post transplant survival froma general medical perspective
714
Absolute Contraindications to Transplant
715
When to refer a COPD patient for lung transplant?
716
When to refer for ILD Lung transplant?
717
When to refer CF to Lung Transplant?
718
When to refer PAH for transplant?
719
Complications post auto-BMT?
EARLY: Infections Diffuse alveolar hemorrhage Post engraftment respiratory distress syndrome Radiation pneumonitis Pulmonary edema Aspiration pneumonitis or pneumonia LATE: Infections Organizing pneumonia Obliterative bronchiolitis PPFE and other ILDs PVOD lesions Malignancy (recurrence or secondary)
720
Complications post allo-BMT?
EARLY: Infections Diffuse alveolar hemorrhage Hyperacute and acute GVHD Pulmonary edema Aspiration pneumonitis or pneumonia LATE: Infections Organizing pneumonia Obliterative bronchiolitis PVOD lesions Malignancy (recurrence or secondary)
721
Risk factors for PGD (primary graft dysfunction)
Age >20 <45 donor African American donor Female donor Donor smoking history Trauma to donor Blood products ECMO used as bridge Recipient diagnosis of IPF, PAH
722
Presentation of PGD (primary graft dysfunction)
Usually within 72 hours Reperfusion injury (the mechanism) Bilateral patchy opacities, ARDS like DAD on pathology
723
How is PGD graded (ISHLT)?
Only GRade 3 has been shown to be associated with poor outcomes
724
Airway Complications of Transplant
* Early (<8 weeks) : infection and dehiscence * Late (>8 weeks): stenosis and bronchomalacia * Need bronchoscopy to diagnose.
725
Difference between Acute Rejection types
* Acute cellular rejection: T cell mediated highly associated with CLAD and decreased immunosuppression * Acute Antibody Mediated Rejection: B cell binding. DSA and AMR associated with CLAD
726
Diagnosis of acute rejection
Cellular: TBBx (Perivascular monoculear infiltrates) Antibody mediated: DSA, TBBx, CD4 staining
727
Histological findings in acute rejection
Perivascular and interstitial mononuclear infiltrates → A score Lymphocytic bronchiolitis → mononuclear cell infiltrates in submucosa of bronchioles → B score
728
Treatment of PGD vs acute rejection
PGD: Supportive, ARDS ventilation Acute: * steroids for all, switching maintenence therapy, anti thymocyte (ATG), Basiliximab * ab mediated no standard of care but PLEX/IVIG often tried with anti thymocyte (ATG)
729
Definition of CLAD
FEV1 decline by >/20% from baseline that lasts for at least 3 months (For definite), and change is not explained by something else (e.g. infection) BOS: FEV1/FVC <0.7 RAS: TLC<90% baseline (or FVC <80% baseline), persistent fibrotic opacities
730
Risk factors for CLAD
Previous PGD or acute reflection Infection, especially CMV, colonization with PsA or aspergillus GERD Aspiration Medication/IST non compliance or underdosed Increased donor age Male to female donor
731
Imaging findings in BOS vs RAS (restrictive allograft)
BOS: mosaic attenuation, centrilobular nodules, gas trapping/hyperinflation, bronchiectasis with time, usually not significant opacities RAS: Pleuroparenchymal fibroelastosis, NSIP
732
Histological findings in BOS vs. RAS(restrictive allograft)
BO: Lymphocytic inflammation of submucosa, intraluminal lesion formation, obliteration of airway RAS: PPFE
733
Treatment for BOS vs. RAS
Address risk factors e.g. GERD Optimize immunosuppression (MMF > Aza, Acro > cyclo) Consider azithromycin (those with neutrophilic BAL especially responsive)
734
Complications post lung transplant
Early: Acute or hyperacute rejection Infectious complications e.g. bacterial, viral, fungal, empyema, surgical site, line infections Bleeding e.g. hemoptysis, hemothorax Dehiscence Anastomotic leak, prolonged air leak Phrenic nerve injury causing diaphragmatic dysfunction Pulmonary embolism, DVT Cardiac arrhythmias Late: Chronic rejection Infectious complications e.g. viral, fungal, bacterial Tracheal stenosis Tracheobronchomalacia Tracheoesophageal and tracheoarterialfistulization Dehiscence PTLD, non melanomatous skin cancer, other malignancies Disease recurrence
735
Timeline for infectious complications post transplant
First month: MRSA, VRE, pseudomonas, candida, HSV Month 1-6: PJP, aspergillus, nocardia, CMV, EBV, endemic fungi, TB, NTM >6 months: Community organisms
736
Examples of post transplant malignancies
PTLD, lymphoma (B cell predominant) Non melanomatous skin cancer Primary lung cancer Breast cancer
737
Causes of PTLD (post transplant lymphoproliferative Disease)
EBV virus, serostatus (highest in R-/D+) Degree of immunosuppression (T cell immunosuppression)
738
Treatment of PTLD
Decrease immunosuppression Rituximab Chemotherapy (CHOP) Surgery/Rads PRN
739
Diseases with recurrence post transplantation
Bronchogenic carcinoma Idiopathic pulmonary hemosiderosis Giant cell interstitial pneumonitis A1AT deficiency (if smoking) PVOD PAP (hereditary cases) LAM PLCH Sarcoidosis → most common DIP Diffuse panbronchiolitis
740
Difference between CMV infection and CMV disease
CMV infection: evidence of active replication and shedding (e.g. antigenemia, PCR, culture) without attributable signs or symptoms - CMV isolation in the blood by viral isolation, rapid culture, antigenemia, QNAT CMV disease: infection with attribute signs or symptoms; can be viral syndrome or tissue invasive disease - CMV isolation in the lung tissue by viral isolation, rapid culture, histopathology, immunohistochemistry - Also CMV PCR in the blood needed
741
Risk factors for CMV post lung transplant
D+/R- (highest risk) D+/R+ D-/R+
742
Risk factors for CMV post allogeneic BMT
R+/-D- Degree of immunosuppression, use of high dose steroids GVHD Prior CMV viremia
743
Treatment of CMV disease
Oral valganciclovir IV ganciclovir Foscarnet is second line treatment Reduction in IST should be considered
744
Congenital causes of non CF bronchiectasis
* Cystic fibrosis * Primary ciliary dyskinesia * Young syndrome ( Men with sinusitis, infertility due to vas deferens obstruction and bronchiectasis) * Williams- Campbell (bronchomalacia with decreases/absent cartilage around subsegmental bronchi. You get cystic bronchiectasis) * Alpha 1 antitrypsin * Yellow nail syndrome * Mouniere Kuhn syndrome (tracheobronchomegaly and lung sequestration * Kartaaganer syndrome ( situs inversus, chronic sinusitis, and bronchiectasis)
745
Cause of PCD
Autosomal recessive Loss of or dysfunctional cilia
746
Clinical manifestations of primary ciliary dyskinesia
Chronic sinopulmonary infection Bronchiectasis Male infertility Situs inversus
747
Kartaganer syndrome
Bronchiectasis Chronic rhinosinusitis Situs inversus
748
Diagnosis of PCD
Low or absent nasal nitric oxide Genetic testing for confirmation Can do sinus biopsy but can be falsely negative
749
Cause of Young syndrome
* Abnormally viscous mucous * Triad of bronchiectasis, chronic rhinosinusitis and infertility due to vas deferens obstruction * Can appear to be similar to CF and primary ciliary dyskinesia (PCD) patients, but they have had normal sweat chloride tests and normal cilia
750
Clinical manifestations of young syndrome
Chronic sinopulmonary infections Bronchiectasis Male infertility
751
Triad for yellow nail syndrome
Yellow nails Respiratory symptoms Lymphedema
752
Most common causes of bronchiectasis
Post infectious Idiopathic Immunodeficiency Connective tissue disorders
753
2 most common causes of non CF bronchiectasis exacerbations
PsA H. influenzae (SA in CF instead)
754
Blood work would you send for everyone with bronchiectasis
CBC IgE, Asp IgG, workup ABPA IGAMs Sputum cultures
755
Imaging findings of bronchiectasis
Signet ring sign/broncho arterial ratio >1 Tram tracking, non tapering peripheral airways Mucous plugging Bronchial wall thickening Gas trapping
756
Airway clearance techniques
* Active cycle of breathing technique * Autogenic drainage * Gravity positioning * OPEP * Nebulized saline * Remember NMD: Lung volume recruitment (LVR) (aka “breath stacking”) Glossopharyngeal breathing Manual resuscitator Mechanical inspiration Mechanical cough assistance Manually assisted cough (MAC) Mechanical insufflator-exsufflator (MIE)
757
Airway clearance techniques that are not recommended
Inhaled mannitol Inhaled NAC Inhaled dornase alpha Carbocysteine
758
Treatments in non-CF bronchiectasis to reduce exacerbations
Airway clearance Pulmonary rehabilitation Mucoactive therapy Chronic abx - azithro for non PsA, inhaled for PsA
759
Abx choices for prophylaxis in those who have recurrent exacerbations
Azithro if non PSA Inhaled anti pseudomonas if PSA - tobra, collistin, gentamicin (or azithro if none of these are tolerateD)
760
When should you offer long term antibiotics to patients with non cf bronchiectasis (how many exacerbations)?
ERS 2017 says >3 per year should be offered chronic Abx. Inhaled for those with PSA+/- macrolide
761
Definition of bronchiectasis exacerbation
Worsening symptoms Over last 48 hours
762
Role of bronchodilators in management of bronchiectasis
LABA in those with significant breathlessness
763
Indications for resection in bronchiectasis
Localized disease not controlled with medical treatment Post obstructive bronchiectasis due to tumors Massive hemoptysis Recurrent exacerbations Overwhelming sputum production
764
Outline possible treatment alogorithm for newly discovered PSA on a sputum in NON-CF bronchiectasis
765
Median age of survival in CF
68 years after Trikafta (2022)
766
Pathogenesis of CF
CFTR transmembrane protein mutation Chromosome 7 gene (long arm) Transepithelial chloride channel Abnormally thick mucus, difficulty clearing, infections and colonization
767
Classes of mutations in CF
* Class 1 – absent or defective protein synthesis * Class 2 – abnormal processing or transport of the protein to the cell membrane * Class 3 – abnormal regulation of CFTR function, inhibiting chloride channel activation * Class 4 – normal amount of CFTR but reduced function (defective conduction) * Class 5 – reduced synthesis of fully active CFTR * Class 6 – decreased stability of fully processed and functional CFTR
768
Bacteria that classically cause colonization in CF
Staphylococcus aureus ** Pseudomonas ** H. Influenza ** Burkholderia cepacia Aspergillus fumigatus NTM Stenotrophomonas
769
Pulmonary manifestations of cystic fibrosis
Bronchiectasis Bacterial colonization Recurrent pulmonary infection Mucous plugging and collapse Pneumothorax Hemothorax Gas trapping and obstruction
770
Extrapulmonary manifestations of cystic fibrosis
Sinus - sinusitis, nasal polyps Intestinal - Meconium ileus, DIOS, SIBO, chronic constipation Pancreas - pancreatic insufficiency with steatorrhea and vitamin ADEK deficiency, chronic pancreatitis, diabetes Liver - transaminitis, biliary cirrhosis, fatty liver disease, cirrhosis Reproductive - male/female infertility; absence of vas differences, thickening of cervical mucus MSK - osteopenia or osteoporosis Depression
771
Causes of abdominal pain in CF
Chronic constipation DIOS (distal intesinal obstruciton syndrome) SIBO (small intestine bacterial overgrowth) Pancreatitis Appendicitis Intussusception Colon cancer
772
Colon cancer screening in CF
Age 40 and q5 years or as dictated by polyp Age 30 if previous transplant
773
Diagnostic criteria for cystic fibrosis → See figure. Tests that can be used to diagnose CF
Clinical: NBS, family history, sx Sweat chloride test Genetic testing Extended CFTR analysis Functional assays
774
Newborn CF screens
* Serum immunoreactive trypsinogen assay (elevated is positive) * DNA assay
775
DDx of positive sweat chloride test
Malnutrition Anorexia, bulimia Pancreatitis Untreated adrenal insufficiency Untreated hypothyroidism Hypophysitis Technical/test factors
776
DDX of negative sweat chloride test
Dehydration Physiologic low sweat rate Hypoproteinemic states Drugs e.g. mineralocorticoids On CFTR modulators (e.g. baby of mother on CFTR modulator during pregnancy) Technical/test factors Malnutrition
777
How to interpret a sweat chloride test in CF
778
What is the difference between CFTR-related disorder and CFTR-Related Metabolic Syndrome.
* CRMS: children with a positive newborn screen AND one of ** Sweat chloride <30 and 2 CFTR mutations of which 1 has unclear phenotypic consequences ** An intermediate sweat chlorid (30-59) and 1 or 0 CF causing mutations * Note: most will not devlop clinical CF and this has been combined with CF Screen positive Inconclusive Diagnosis (CFSPID) * CFTR-Related Disorder: Do not meet diagnostic criteria for CF or CRMS but are affected by CF related Conditions.
779
CF management
Smoking cessation, vaccinations Airway clearance, bronchodilators Inhaled hypertonic saline Inhaled DNAse Chronic azithromycin +/- modulator therapy
780
Airway clearance techniques for patients with CF
Active cycle of breathing Autogenic drainage Positional therapy Oscillating PEP device - Aerobika, Acapella, flutter valve Percussive vest
781
Risk factors for acquiring MRSA
Younger F508 delta Higher admissions PsA co infection
782
Role of abx in CF
Eradication Prevent exacerbations Exacerbation
783
Indications for eradication abx therapy in CF
PsA +/- MRSA
784
Abx that can be used to treat chronic PSA or PSA eradication
Aztreonam 500 mg oral MWF Tobramycin 300 mg nebulized BID Colistin 150 mg nebulized BID Aztreonam 75 mg nebulized TD * weak evidence 28 days on and off
785
Indication for eradication abx and how to do it with PSA in CF.
786
Abx choices for CF exacerbation
MSSA: amoxi-clav, doxy, septra - cefazolin, nafcillin MRSA: Septra, doxycycline - Vancomycin, linezolid PsA: cipro - ceftaz, piptazo, mero, tobra, aztreonam Steno: septra, doxy, levoflox - ceftaz, colistin
787
Duration of treatment for CF exacerbation
At least 2 weeks but often longer
788
Definition of massive hemoptysis in CF
Scant <5 cc Mild to moderate 5-240 cc Massive >240 cc
789
Management of hemoptysis in CF
Scant: +/- abx, continue everything Mild/moderate: stop HS, no consensus DNAse, airway clearance; START abx Massive: stop HS, airway clearance, no consensus DNAse; START abx Stop BiPAP if on it (unless mild)
790
Add-on options for ongoing hemoptysis
Vitamin K, tranexamic acid Bronchial artery embolization Lung resection Transplantation
791
Management of pneumothorax in CF
No consensus re antibiotics Follow guidelines re: chest tube Hold percussive therapies (including PEP devices) Hold BPAP Do not withhold mucous clearance and aerosols
792
Indications for pleurodesis
Not after first episode After recurrence Surgical pleurodesis is preferred
793
Recommendations post PNTX inCF
No travel x 2 weeks after resolution No heavy lifting 5 lb x 2 weeks after resolution No spirometry x 2 weeks after resolution
794
Different types of mutations in CF
Class I: Nonsense mutation, Decreased synthesis Class II: processing mutation e.g. F508del Class III: Gating mutation e.g. G55D, Class IV: Conductance e.g. R117H Class V: Decreased production Class IV: Decreased stability
795
Who is eligible for CFTR modulator therapy?
F508 del Gating mutation e.g. G551D R117H
796
Benefits of CFTR modulator therapy
Improve symptoms Improve quality of life Improved lung function/FEV1 (10.4%) Improved weight Improve sweat chloride Reduced exacerbation and admission Improved mortality
797
What is the most common NTM in CF?
MAC complex
798
How often do you screen patients with CF for NTM?
Annually in spontaneously expectorating Do not need to go hunting for sputum if not spontaneously expectorating and no sx Do not use oropharyngeal swabs
799
Treatment of hemoptysis during bronchoscopy
Cold saline Topical epinephrine 1:10,000 Bronchial blocker Wedge with bronchoscopy Lateral decubitus Intubate
800
Benefits of BCG vaccine
Prevent CNS tuberculosis. Prevents disseminated TB. Protection is mainly during childhood (up to age 15)
801
Organisms are in the mycobacterium TB complex
Mycobacterium tuberculosis Mycobacterium bovis Mycobacterium carnetti Mycobacterium africanum Mycobacterium microti
802
Risk factors for developing primary infections? (18-24 months post is still considered primary disease)
Age <5 Immunocompromised e.g. HIV
803
Risk factors for CNS TB
Age <5 HIV
804
Risk factors for tuberculosis
Contacts e.g. household contacts Birth in TB endemic area Immunosuppression Substance abuse Socioeconomic status Malnutrition Certain systemic diseases e.g. COPD, DM, silicosis, renal disease, malignancy
805
How long after exposure does it take to develop positive TBST or IGRA?
3-8 weeks
806
Risk factors that increase the probability of TB transmission
Cavitary disease Upper lung zone disease Laryngeal disease AFB smear positive disease Level of exposure - proximity, time spent with them, environment Coughing, sneezing
807
Modes of transmission of TB
Airborne Droplet Percutaneous Ingestion
808
Isolation in TB
Smear negative → 2 weeks Smear positive → 2 weeks if 3 consecutive smear negative AFB Smear positive → 4 weeks if persistently positive sputums For rifampin resistance, 4 weeks +/- 3 negative smears
809
Indications for hospitalization inTB
Complicated TB, comorbid conditions Has acute complication of TB e.g. hemoptysis Drug desensitization Is non compliant with medication Cannot isolate safety at home
810
What conditions must be met for someone isolating at home?
No shared ventilation with other units (non household members) Everyone in household has already been exposed and if TBST negative, should accept risk of ongoing exposure <5 or immunocompromised patients are already on treatment for latent or active TB
811
Differences in treating TB in HIV
Longer duration IF NOT ON ART Rifampicin rather than rifampin Consideration of timing of ART therapy +/- steroids
812
Imaging findings of primary TB
Lower lobe distribution Parenchymal consolidation - Opacities, GGO, tree in bud nodules May have cavities Miliary TB Hilar, mediastinal LN →RML collapse More likely to have pleural effusion
813
Imaging findings of secondary TB
Upper lobe distribution (apical, posterior > sup segment > anterior) Consolidation, tree in bud Cavitation 5% have upper lobe fibrocalcific changes
814
Latent TB testing is not required in these situations
Low pretest probability Diagnosis of active TB in those >12 years old Trending response to treatment Mass testing programs for e.g. immigrants (not including HCW/occupations)
815
Indications for latent TB testing?
CXR showing apical fibronodular changes typical of healed TB Recent exposure to active TB Certain occupations e.g. HCW, prisoner workers, shelter workers HIV (any stage) IVDU or use of illicit drugs Post HSCT or organ transplant (and pre transplant workup) On immunosuppressive therapies (includes chemo) Lymphoma, leukemia, head and neck cancers Chronic kidney disease requiring dialysis Silicosis
816
What immune response does the TBST depend on?
Type IV delayed type hypersensitivity
817
TBST preferred over IGRA when:
Contact tracing Serial testing HCP and others
818
Serial testing is required in TB when:
Contact investigation Serial testing of HCW, other populations e.g. inmates, prison workers
819
IGRA is preferred when:
Unclear if patient will return Children >10 received vaccine after age 1, unclear when, >/2 vaccines Children >2 but <10 previously received vaccine Adequate training, personnel, facility for TBST not available TBST is contraindicated Previous known NTM infection
820
Contraindications to TBST
Previous allergic reaction, blistering reaction
821
Causes of false positive TBST
Technical limitations Prior vaccination Sensitization to NTM (not an issue with IGRA) Rupture of venule at time of injection
822
Causes of false negative TBST
Technical limitations HIV Active TB or fungal infection Live virus vaccine in the last 4 weeks Recent infection Steroids >/15 mg x >2-4 weeks Natural waning of immunity
823
Causes of false negative IGRA
Immunosuppression e.g. HIV, active TB Technical variability
824
Sensitivity of TBST vs IGRA for latent TB
TBST: 77% IGRA: 60-95%
825
Indications for both IGRA/TBST
Either can be done to increase sensitivity after negative test IGRA can be done after positive TBST to increase specificity
826
Cutoffs for positive TBST - See table
<5 >/5 >/10
827
Available tests to assess for TB
AFB smear (Zeil Nielson, Auramine Rhodamine) - sensitivity 20-80% PCR - sensitivity 70-95% Culture Histopathology
828
Diagnosis of active TB
Appropriate clinical and imaging findings Positive TB culture, positive TB PCR +/- AFB
829
Samples that can be collected for diagnosis of TB
Sputum Induced sputum BAL Tissue Urine (guideline recommends against lipoarabinomannan but can still do culture) Blood Gastric aspirate Stool
830
Pathological findings in tuberculosis
Caseating granulomatous inflammation May see organisms, may stain positive for AFB
831
DDX for positive AFB stains
Tuberculosis NTM, most likely MAC Nocardia Rhodococcus Actinomyces
832
What percentage of patients with latent TB will develop active TB in their lifetime?
5-10% 50% of that risk is in the first 2 years Canadian specific can use TSTin3D (McGill online calculator) to estimate the cumulative risk of disease for active TB
833
Drug regimens for the treatment of latent TB
3HP = isoniazid and rifapentine weekly x 3 months (First Line) Rifampin daily x 4 months (First line) Isoniazid daily x 9 months (Second Line) Isoniazid daily x 6 months (Alternative) Isoniazid and rifampin daily x 3 months (alternative)
834
Pretreatment testing before latent TB treatment
Assess for active TB - CXR → sputum AFB if CXR is abnormal LFTs Creatinine CBC HIV, hepatitis B, hepatitis C
835
Indications to treat pregnant patients with latent TB
Recent close contact with active TB On immunosuppression Has HIV
836
Treatment of pregnant patients with latent TB
Rifampin x 4 months
837
Treatment of non-resistant active TB - What are their benefits?
Isoniazid 5 mg/kg daily → prevent resistance - bactericidal Rifampin 10 mg/kg daily → prevent resistance, relapse - bactericidal Ethambutol 15 mg/kg daily → prevents resistance Pyrizinamide 20 mg/kg daily - bactericidal FQ (moxi/levo) when person has A/E requiring cessation of a first line drug
838
Preferred Treatment and alternatives treatments for active TB (TB disease)
* isoniazid, rifampin, pyrazinamide and ethambutol daily for the first 2 months followed by isoniazid and rifampin for 4 more months * Suspected susceptibility: ** RIPE daily x 2 months then RIE daily for 4 months * Known susceptibilities: ** RIP daily x 2 months then RI daily x 4 months * Note: should add pyridoxine (Vit B6) 25-50mg/day for all those takine INH at risk for peripheral neuropathy ** people with diabetes, chronic kidney disease, human immunodeficiency virus (HIV) malnutrition, seizure disorder or a history of substance misuse, as well as pregnant or breastfeeding women
839
Alternative treatment regimens for active TB
R/I/E x 2 months then extend out to 7 months Can also do the drugs in continuation phase (whether R/I or R/I/E 3 times per week)
840
Treatment with drug-susceptible pulmonary TB and what are the risk factors for relapse
extensive disease OR baseline cavitary disease on x-ray and smear or culture positive sputum at two months) extension of the continuation phase to seven months for a total of nine months of TB drug therapy (poor evidence).
841
What do you do if a patient is missing tb treatment doses?
842
Potential side effects of TB treatment
Isoniazid - peripheral neuropathy, hepatic toxicity, drug induced SLE Rifampin - drug-drug interaction, body fluid discolouration, hepatic toxicity, rash Ethambutol - optic neuropathy, red-green color blindness Pyrazinamide - hepatotoxicity
843
Examples of drug-drug interactions with rifampin
DOACs, warfarin Oral contraceptives Antifungals Tacro, cyclo Methadone Phenytoin
844
When should you be concerned about liver toxicity with TB drugs?
Billi >3, serum, ALT > 3 ULN with sx, ALT >5 ULN with no sx Can continue ethambutol; consider adding FQ Discontinue, restart slowly with careful monitoring Obviously assess for other causes of transaminitis
845
Indications to extend active TB treatment to 9 months
BASELINE Cavitary ON CXR + smear/culture positive at 2 months Diabetes and cavitary disease HIV not on ART therapy Solid organ transplant recipients On TNF alpha inhibitors Did not use pyrazinamide in intensive phase TB meningitis TB bone disease if elevated inflammatory markers at end of 6 months
846
When do you start ART therapy in a patient with active TB and HIV?
TB meningitis or CD4>50- delay until after 2 weeks of starting TB therapy **Out of concern for Immune REconstitution Inflammatory Syndrome (IRIS) No TB meningitis and/or CD4 <50 - within 2 weeks of starting TB therapy Pred 40 x 2 weeks if CD4 <100, unless active hepatitis B, kaposi, rifampin resistance
847
What is IRIS and how does it manifest?
Immune REconstitution Inflammatory Syndrome (IRIS) Lymph node enlargement and pulmonary infiltrates. Usually self limited but can warrant steroids.
848
Monitoring patients with active TB on treatment
CBC, crea, LFTs monthly HIV, hepatitis B/C at start of treatment CXR at baseline, then q2 months Sputum smear, culture q2 weeks until smear negative; then 2 and 1 month before end PFT within 6 months of finishing treatment
849
Recurrence vs relapse vs reinfection
Recurrence: can be due to either Relapse: same strain Reinfection: different strain
850
Risk factors for recurrence of TB
Cavitary disease, smear positive disease Extensive or disseminated disease Drug resistant disease Immunosuppressed Intermittent therapy (not daily), treatment interruptions Was not adherent Should monitor these patients for 12-24 months with sx/imaging/microbiological testing
851
Treatment of active TB in pregnancy
RIE (omit P) x 9 months
852
Indications to give pyrazinamide in pregnancy
Smear positive Extensive disease Disseminated Intolerance to any first line drugs
853
Drugs that are contraindicated in pregnancy (TB)
+/-PZA All injectables Fluoroquinolones
854
Common locations for extrapulmonary tuberculosis
Pleural* Abdominal* Lymphadenopathy* CNS - tuberculoma, CNS meningitis Bone - vertebral disease, arthritis Cutaneous Genitourinary Ocular
855
Definition and diagnosis of disseminated TB
Disease in >?2 non contiguous organs OR isolation in blood, bone marrow, or liver on bx Milliary TB is subset of disseminated TB
856
Differential diagnosis for miliary pattern on CT
Disseminated tuberculosis Other infections: histoplasmosis, mycoplasma, varicella Sarcoidosis, pneumoconiosis, amyloidosis Miliary metastases e.g. thyroid cancer, breast cancer, RCC, melanoma
857
Tests that can help assess for TB Pleuritis
Fluid analysis Fluid adenosine deaminase Fluid interferon gamma Fluid AFB and culture Histopathology
858
Fluid characteristics in TB pleuritis
Low - normal glucose pH >7.3 LDH >500 Neutrophil predominant early on, the lymphocyte predominance <5% mesothelial cells Pseudochylothorax, chylothorax
859
Treatment of pleural TB
RIPE x 6 months Chest tube if empyema, may need decortication No steroids No therapuetic thoracenteisis/chest tube for pleural TB associated effusions.
860
Extrapulmonary TB cases that require extended therapy
CNS x 9-12 months, requires higher doses of rifampin >15 mg/kg Joint x 9-12 months if markers of severity at 6 months (CRP, ESR)
861
Imaging findings in CNS TB
Basal leptomeningeal enhancement Hydrocephalus Infarcts
862
Benefits of steroids in the treatment of TB meningitis
Mitigate increased ICP, reduce hydrocephalus and infarction, reduce short term mortality Does not affect disabling neurological consequences or long term survival
863
Steroid regimen in the treatment of TB meningitis
120 mg x 1 week 90 mg x 1 week 60 mg x 1 week 30 mg x 1 week 15 mg x 1 wek 5 mg x 1 week
864
Treatment of TB pericarditis
RIPE x 6 months Steroids in HIV negative NOT HIV positive (ART or no ART)
865
Indications for steroids in the treatment of TB
Treating TB in HIV with CD4 <100 to prevent IRIS (Only if on HAART) All patients with meningitis HIV negative patients with pericarditis (No recommendation for or against if HIV+ on therapy with HAART and have TB pericarditis)
866
Definitions of TB resistance
Monoresistant: Resistant to any of the first line therapies. Poly drug resistance: Resistant to 2 of the first line therapies (not rifampin) MDR: Resistant to INH + Rifampin with/without resistant to other first line agents. Pre-XDR: MDR TB with additional resistance to any FQ. XDR: Pre-XDR + resistance to bedaquiline/linezolid
867
Treatment of MDR-TB
initial regimen should include levofloxacin or moxifloxacin AND bedaquiline AND linezolid AND clofazimine AND cycloserine. 5 to 7 months after culture conversion occurs, the total number of drugs in the regimen can be reduced to 4 for a total duration of 18-20 months.
868
Treatment of pre-XDR or XDR
Same as MDR. Ensure 5 drugs in the regimen initially. Cannot use resistant drugs. In order of preference add on: ethambutol, pyrazinamide, delamanid, amikacin, imipenem-cilastatin or meropenem (plus clavulanic acid), ethionamide and p-aminosalicylic acid.
869
Is surgery indicated in MDR-TB
Partial lung resection in carefully selected patients can be used as an adjuvant. Optimally after culture conversion is achieved.
870
Which Countries have the highest incidence of TB and MDR (According to WHO)
TB: Philippines, Pakistan, Somalia, India MDR: Somalia, China
871
Most common NTM species to cause infection
MAC M. Kansassi M. abscessus
872
Modes of transmission for NTM
Soli aerosols(All but M. Kansasii) Water aerosols Soft tissue Aspiration
873
Risk factors for development of NTM
Older age Female Lower BMI Thoracic cage abnormalities, mitral valve prolapse Immunocomp (e.g. HIV, IST, malignancy) but can happen in immunocompetent too Underlying structural lung disease e.g. bronchiectasis, CF, ILD, COPD/asthma Oral steroids >15 mg/day Inhaled fluticasone >800 mcg/day Anti TNF alpha
874
Risk factors for progression of NTM
Older age Male Lowe BMI Immunosuppression - primary immunodeficiency, HIV infection, IST, anti TNF, steroids? Labs: elevated ESR/CRP, hypoalbuminemia Fibrocavitary disease Extent of disease Bacterial load and species and smear positivity
875
2 pulmonary phenotypes that are produced by NTM
Fibrocavitary Nodular bronchiectatic Other: HP, solitary pulmonary nodule, disseminated
876
Non pulmonary manifestations of NTM
Superficial lymphadenitis (especially cervical) Skin and soft tissue infection Disseminated disease
877
Radiographic findings of NTM
Fibrocavitary - thick walled cavities, upper lobe predominance Nodules, tree in bud nodularity Bronchiectasis GGO, centrilobular nodules, gas trapping in HP
878
What other features are seen in Lady Windermere syndrome?
Scoliosis Pectus excavatum Mitral valve prolapse
879
Diagnostic criteria for NTM → See table.
Symptoms Imaging consistent with pulmonary disease Exclusion of other diagnoses 2 sputum or 1 BAL If M. abscessus should be speciated ot the subspecies level and checked for macrolide resistance. OR if disseminated x1 blood culture/culture from site of infection
880
What is special about the sputum cultures that are obtained in NTM diagnosis vs TB?
TB - 3 sputums, 1 hour apart is fine NTM - 2 sputums, same species/subspecies should be isolated over interval of >/1 week
881
If monitoring patients with NTM instead of treating, how and how frequently do you monitor them?
Sputum culture q2-3 months Repeat imaging after 6 months
882
When do you treat NTM?
2020 guidelines say treat if diagnosed instead of watchful waiting. (condition and very low evidence) Especially treat if: Positive smear or cavitary disease
883
What is the treatment for NTM? other than Abscessus See table.
* Note rifampicin and rifampin are the same thing * MAC should ** always have a azithromycin if susceptible and if cavitary/macrolide resistant/refractory should have amikacin or streptomycin addedd **Treated 12 months post conversion * Kanasii ** Rifampin susceptible suggest Rifampin, Ethambutolo and either INH or azithro (daily is preferred in most cases) ** Rifampin resistant then add moxifloxacin ** Treated for at least 12 months (regardless of conversion) * Xenopi ** Moxi or Azithro with a total of minimum 3 drugs. ** If cavitary or adanced add amikacin ** Treat 12 months beyond conversion
884
How do we treat NTM Abscessus?
Abscessus * There is an initial and continuation phase and you need to know if it is Mutational susceptible and inducible susceptible (14 days). * Need 3 active drugs initially * duration - “short vs. long”-Expert opinion
885
What is the definition of refractory disease in NTM?
Culture positive after 6 months
886
What makes treatment of abscessus unique?
Can have chromosomal mutations Mutation and inducible resistance
887
Treatment categories for MAC
Fibronodular disease Extensive disease/cavitary disease Macrolide resistant disease Refractory disease
888
Treatment categories for Kansasii treatment
Fibronodular disease Extensive disease/cavitary disease Rifampin resistance
889
Treatment categories for Xenopi treatment
Fibronodular Extensive/cavitary disease
890
Indications for surgical management
Severe complication e.g. hemoptysis Not responding to medical therapy, refractory disease
891
Duration of treatment for MAC, Kansasii and Xenopi
MAC x 12 months post first negative culture/culture conversion Kansasii x 12 months fixed Xenopi x 12 months post culture conversion Abscessus - expert opinion
892
Which fungi require T cell mediated defense vs phagocytosis?
T cell mediated immune defense: PJP, endemic fungi, NTM/TB, crypto Phagocytosis: candida, aspergillus, mucormycosis
893
Disease manifestations of aspergillus
ABPA Aspergillus nodule Aspergilloma - unusual to be caused by other fungus Chronic cavitating pulmonary aspergillosis Chronic fibrosing pulmonary aspergillosis Semi invasive pulmonary aspergillosis Invasive pulmonary aspergillosis Tracheobronchitis
894
Available aspergillus microbiological testing
Aspergillus IgG - most sensitive IgE specific Aspergillus for ABPA) Serum/BAL - PCR Serum/BAL - galactomannan Sputum/BAL/tissue/blood/other - culture
895
RFs for chronic cavitation aspergillosis
Pre-existing structural lung disease. COPD Tuberculosis Cystic fibrosis Others
896
Risk factors for invasive pulmonary aspergillosis
Prolonged neutropenia <500 for >10 days (biggest risk) Transplantation - lung, HSCT Hematological malignancy Steroids >3 weeks Chemotherapy HIV/AIDs Chronic granulomatous disease
897
How do you generally diagnose chronic pulmonary aspergillosis?
At least 3 months in duration Consistent clinical and imaging features Evidence of Asp IgG vs positive sputum/BAL/biopsy culture
898
Imaging findings for invasive aspergillosis
Nodules Reverse halo sign (more common with OP and less commonly fungal but mucormycosis most common of the fungal) Atoll sign (same as reverse halo sign) Halo sign is most commonly associated with IPA Air crescent sign (delayed finding) Wedge shaped infarcts Tree in bud opacities
899
Treatment for a pulmonary aspergilloma
Single - can observe or surgery/embolization if symptomatic Multiple - antifungals (itraconazole) Can give antifungals pre/post surgery if high risk spillage
900
Treatment of chronic cavitary pulmonary aspergillosis
Observe Itraconazole, vori, posi x 6 months
901
Treatment for invasive pulmonary aspergillosis
Voriconazole IV first then po x >/6 weeks need radiographic/clinical improvement. Can also transition to po itroconazole.
902
Imaging findings for ABPA
Finger in glove, mucous plugging Mucous plugging can cause collapse Bronchial wall thickening Central bronchiectasis Fleeting pulmonary alveolar opacities, usually upper lobes Pulmonary fibrosis in chronic disease
903
diagnostic criteria for ABPA - new criteria
904
Treatment for ABPA
Prednisone 0.5mg/kg x 2-4 weeks then taper to complete over 4 months OR itraconazole for 4 months Itraconazole x 16 weeks/voi/posi (old) Do not use high dose ICS for treatment purposes Do NOT recommend Anti-IL5 agent as first line (nt confirmed by RCT yet) Prednisone Itraconazole x 16 weeks/voi/posi Anti-IL5 agent (not confirmed by RCT yet)
905
Treatment of ABPA exacerbation
New treat same as Anewly diagnosed ABPA (pred or itraconazole) but no biologic MIld → ICS (No) More than mild → increase oral steroids If refractory (>/=2 in last 2 years) can combine pred adn itraconazole)
906
Treatment response
Improvement in 8-12 weeks of: * Chest radiograph * IgE level (20% fall) * Clinical symptoms. NOTE: aspergillus IgE and IgG levels or eos may not fall so don’t recheck for response.
907
Risk factors for disseminated disease of endemic Fungi?
Medications e.g. TNF-alpha inhibitors, steroids, IST HIV/AIDs Immune disorders e.g. CVID Hodgkin’s lymphoma Extremes of age
908
Pulmonary manifestations of histoplasmosis
Acute localized pulmonary histoplasmosis Diffuse pulmonary histoplasmosis Chronic pulmonary histoplasmosis Disseminated histoplasmosis
909
Radiographic manifestations of histoplasmosis
Acute localized pulmonary histoplasmosis - Local infiltrates/pneumonitis (usually lower) Diffuse pulmonary histoplasmosis - Reticulonodular - Miliary Chronic pulmonary histoplasmosis - Apical fibrocavitary Disseminated histoplasmosis - Miliary
910
Manifestations of chronic pulmonary histoplasmosis
Apical infiltrations, fibrosis Cavitation Fibrosing mediastinitis Mediastinal granuloma Can send secondary infection of cavitation Broncholithiasis
911
Diagnosis of different manifestations of histoplasmosis
Use antigen (urine*, blood, BAL) + antibody for acute disease (local or diffuse) or disseminated disease Use culture (BAL, TBBx) for chronic disease - sputum sensitivity is low Mediastinal disease: ab usually positive; antigen -, culture
912
Histopathology of histoplasmosis
Small yeast with narrow based budding
913
Treatment of mediastinal manifestations of histoplasmosis
Broncholithiasis → observe, bronchoscopic preferred, surgical Mediastinal granuloma → observe, surgical removal if needed Fibrosing mediastinitis → stent if needed, no antifungals or steroids (unless sarcoid or vasculitis causing it, then can be trialed)
914
Manifestations of pulmonary coccidioidomycosis
Local primary Diffuse pulmonary coccidioidomycosis Chronic fibrocavitary disease Disseminated
915
Diagnostic criteria for coccidioidomycosis
Combination of tests Antigen (urine, serum, BAL) Antibody (EIA preferred) Direct visualization (sputum, BAL, bx material), path - can see spherules Culture
916
Manifestations of pulmonary blastomycosis
Acute focal pulmonary blasto Acute diffuse pulmonary blasto Chronic pulmonary blasto Disseminated
917
Extra pulmonary manifestations of blasto
Brain Bone - OM Cutaneous - crusting, verrucous lesion GU tract
918
Diagnostic criteria for blasto
Combination of tests Antigen Antibody Direct visualization, path Culture - gold standard
919
Imaging findings of PJP
* Reticular changes, perihilar distribution (more often upper lobe) * Crazy paving (also smooth septal thickening) * Pneumatoceles * Less commonly nodular pattern (granulomatous PJP) * Often hypoxemia is out of proportion to degree of radiographic findings
920
General blood work to assess for PJP
LDH - sensitive Beta D glucan - sensitive
921
Causes of positive beta d glucan
* Pseudomonas infection * IVIG or olther blood products/albumin * IHDialysis using cellulose membrane * Presence of invasive fungal infection (candida, aspergillus,fusarium, histoplasmosis, PJP). ** Not mucormycosis.
922
When is beta d glucan usually negative?
Mucormycosis Cryptococcus Blastomycosis False negative: Hyperpigmented serum (bilirubin or triglyceride elevation) False negative: azitrhomycin or IV pentamidine
923
Diagnosis of PJP
Stained respiratory specimens - sputum, BAL - very sensitive in HIV (97% vs 50-60% HIV -) PCR - blood, sputum, BAL - especially useful in HIV - (Sensitivity up to 100% but 20% of normal population colonized) Beta D Glucan (serum) sensitive in HIV (BHIVA 2024)
924
Treatment of PJP
Septra x 21 days, 15-20 mg/kg IV of TMP component Alternatives: IV pentamidine, primaquine + clinda, atovaquone, dapsone + septra Plus steroids
925
Indications of treating PJP with steroids
PaO2 <70 mmHg A-a gradient >/35 mmHg U2D: SpO2 <92% Most effective within 72h of treatment initiation Steroid Regimen (Classic) Prednisone 40 mg BID days # 1-5. Prednisone 40 mg daily days #6-11. Prednisone 20 mg daily days #12-21. Hg U2D: SpO2 <92%
926
Indications of PJP prophylaxis in HIV
CD4 <200 (continue until >200 for >3 months) CD4 <14%
927
Options for PJP prophylaxis
Septra SS, DS Pentamidine Dapsone Atovaquone
928
Risk factors for invasive candidal infection
Neutropenia Immunosuppression Broad spectrum abx use Necrotizing pancreatitis TPN CVC Intra abdominal surgical procedures
929
Risk factors for mucormycosis
Diabetes, especially DKA Iron overload, deferoxamine tx Hematological malignancies, HSCT, SOT Glucocorticoid treatment COVID-19 pneumonia neutropenia
930
Imaging findings of mucormycosis
Like IPA More pleural effusion atoll sign more than halo
931
Diagnosis of mucormycosis
Culture (usually negative) Histopathology*
932
Treatment of mucormycosis
Liposomal Amphotericin B Surgical debridement IV isavuconazole and IV/PO posaconazole also now recommended as an alternative first line.
933
Risk factors for the development of nocardia
HIV CD4<100 SOT, especially lung - High steroids independent RF - High CNI levels independent RF - CMV in last 6 months independent RF Long term steroids, other IST Lymphoma PAP COPD, bronchiectasis
934
Extra pulmonary manifestations of nocardia
Brain - abscess, meningitis Skin - abscess Bone Muscle
935
Imaging findings of nocardi
Nodule LN rare
936
Teatment of nocardia
Septra Imipenem Cephalosporins 3rd generation Amikacin
937
Treatment duration for nocardia
6-12 months normally 12 months at least if immunosuppressed
938
Compare and Contrast Nocardiosis and Actinomycosis
939
Treatment of Nocardiosis
* Mild or moderate pulmonary disease septra x 6-12 months * Severe: ** Septra IV + amkacin 7.5mg/kg ** OR Imipenem + Amikacin * IV therapy if required is for at least 6 weeks then PO for 6-12 months ** Po options include Septra +/- either minocylcine or amox clav.
940
Treatment of Actinomycosis
* Mild-Moderate ** Oral pen V 2-4g divided into q6 dosing ** Alternative: amoxicillin or Amox clav. * Severe: IV peng G 10-20million units divided into q6h dosing ** CTX is alternative * Duration: ** mild -Moderate 2-6 months ** SeverE: 6-12 months
941
Causes of unilateral hyperlucent lung
Poland syndrome (a congenital unilateral absence of the pectoralis major and minor muscles and is a recognized cause of unilateral hyperlucent hemithorax) Mastectomy Pneumothorax Pulmonary embolism - Westermark Vascular pruning Swyer james mcleod syndrome ( unilateral hemithorax lucency as a result of postinfectious obliterative bronchiolitis often adenovirus or mycoplasma pneumoniae) Congenital lobar emphysema CPAM Giant bullous disease Pneumatocele Pneumonectomy
942
Imaging features of bronchial atresia
LUL predominantly Mucous filled atretic bronchial stump Hyperlucent lung due to hyperinflation of distal lung (Pores of Kohn) Bronchial atresia is a developmental anomaly characterized by focal obliteration of the proximal segment of a bronchus associated with hyperinflation of the distal lung.
943
Imaging features of CLE (Congenital lobar Emphysema)
Unilateral hyperlucent lung Larger affected lung Decreased vascularity Contralateral mediastinal shift
944
Complications of CLE( Congenital Lobar Emphysema)
Recurrent pneumonia Cyanosis Failure to thrive
945
Imaging features of CPAM(Congenital pulmonary airway malformation)
Type 1 (Most common 70% ) and 4 -1 or 2 large cysts - associated with malignancy Type 2 - small mixed solid/cystic lesions with 90% associated to bronchial atresia Type 3 - numerous small cysts solid or mixed Technically there is a Type 0 but though are very rare and are lethal at birth
946
Indications for treatment of CPAM
Symptomatic Asymptomatic but: - >20% hemithorax - Concern for malignancy - Frequent complications
947
Difference between CPAM and Bronchopulmonary sequestration?
BPS has no connection to the tracheobornchial tree and receives its blood supply from systemic ciculation vs. CPAM gets its blood supply via pulmonary circulation
948
Imaging features of ILS (intralobar sequestration) and ELS (extralobar sequestration)
Both Predominantly LLL Dense mass, sometimes with cystic areas Both systemic feeding vessel
949
Differences between intralobar and extralobar sequestration
Epidemiology (ILS 1:1 ; ELS Male 3: 1) Blood supply ( both from systemic circulation but ILS drains to pulmonary veins and ELS to systemic and is fed from smaller vessels) Location (ILS 60% left base ELS 90% Left with most associated with posterioro congenital diaphramatic hernia) Pleural supply Connection with tracheobronchial tree (ILS has no connection directly but may have bronchopulmonary foregute malformation, ELS does not) Clinical presentation (ILS most likely infections, ELS is asymptomatic through life)
950
Surgical indications for pulmonary sequestration
Symptomatic Complications >/20% of the hemithorax Characteristics concerning for malignancy/pleuropulmonary blastoma
951
Imaging abnormalities in Scimitar syndrome
Anomalous pulmonary venous return - (tubular structure)* Right lung hypoplasia* Pulmonary artery hypoplasia* Ipsilateral mediastinal shift Dextroposition Pulmonary sequestration
952
Causes of tracheobronchomalacia
Previous prolonged intubation Previous tracheostomy Previous surgery e.g. lung transplantation Marfan’s syndrome, Ehlers danlos syndrome, scoliosis, pectus excavatum Relapsing polychondritis, other autoimmune conditions Chronic inflammation e.g. CF, bronchiectasis Recurrent infections e.g. bronchitis Multinodular goiter, malignant or benign lesions of neck and mediastinum COPD, asthma, obesity
953
Diagnostic criteria for tracheobronchomalacia
Non contrast dynamic CT and bronchoscopy (gold) <70% normal, 70-80 mild, 80-90 moderate, >90% severe
954
Treatment for tracheobronchomalacia
Treat underlying cause PAP therapy Airway clearance techniques Stent trial → tracheobronchoplasty (really just focal and proximal tracheobronchial malacia)
955
Diagnostic criteria for tracheobronchomegaly
Trachea >3 cm RMS > 2.4 cm LMS >2.3 cm
956
Causes of tracheal and subglottic stenosis
Congenital and idiopathic Previous intubation Previous tracheostomy Previous surgery e.g. lung transplantation Inflammatory e.g. relapsing polychondritis, vasculitis, sarcoidosis, IgG4 disease, Ra, SLE, amyloidosis Infectious e.g. tuberculosis, fungal, bacterial Malignancy Radiation
957
Management of tracheal stenosis
Treat underlying cause Balloon dilatation Laser cautery Stenting Surgical
958
Causes of tracheal thickening
* Post intubation, post trauma, post surgery * Malignancy e.g. SCAMM ( da fuq? But squamous cell carcinoma is most common) - maybe they meant it as an acronym… ) * * Squamous cell carcinoma * * Chondrosarcoma * * Carcinoid tumour * * Adenoid cystic carcinoma * * Mucoepidermoid carcinoma * * Metastatic disease * Infectious - e.g. TB * Inflammatory - e.g. RP, GPA, amyloidosis, sarcoidosis * Other - e.g. TBM, TBP OCP
959
Causes of thickening spare the posterior membrane
TBM TBPOCP (tracheobronchopathia osteochondroplastica - nodules of cartilage or bone in the submucosa along the tracheal rings) Relapsing polychondritis (inflammation of cartilage in the body)
960
Benign causes of tracheal masses
Chondroma ( slow growing made of cartilage) Leiomyoma (fibroid, smooth muscle tumor) Lipoma Amyloidoma Squamous cell papilloma Hamartoma Hemangioma Tracheobronchomalacia osteochondroplastica -Nodules of cartilage or bone in the submucosa along the tracheal rings)
961
Malignant causes of tracheal masses
Squamous cell carcinoma Chondrosarcoma Carcinoid tumour Adenoid cystic carcinoma Mucoepidermoid carcinoma Metastatic disease SCCAMM
962
Differential diagnosis for mediastinal masses
Anterior - Teratoma - Thymoma and other thymic tumors - Thyroid - goiter, malignancy - Terrible lymphoma Middle - 3A’s - Adenopathy - lymphoma, sarcoid, silicosis, castleman’s, meds, infxn - Aneurysms - aortic aneurysm, fistulas - Anomalies - bronchogenic cyst - Other - lipomatosis, lymphangiomas, hernias Posterior - Neural tumors e.g. Schwannoma, neuroblastoma - Esophageal process e.g. mass, diverticula - Descending aortic aneurysm - Extramedullary hematopoiesis - Bochdalek hernia
963
Blood work in the assessment of teratoma
Beta HCG AFP LDH
964
Examples of thymic tumors
Thymoma Thymic carcinoma Thymic lymphoma Thymic neuroendocrine (carcinoid tumour) Thymolipoma
965
Differentiate a seminoma GCT vs nonseminoma GCT
Beta HCG is high, AFP normal in seminoma Both high in non seminoma
966
Complications associated with fibrosing mediastinitis
Atelectasis & Recurrent infections, dyspnea, cough SVC syndrome Pulmonary hypertension Dysphagia Phrenic nerve paralysis
967
Causes of congenital hernias
Morgagni hernia (Anterior, asymptomatic) Bochdalek hernia (More common, posterolateral, can cause newborn symptoms due to lung hypoplasia) - “Bochdalek is Back”
968
Pulmonary manifestations of relapsing polychondritis
Tracheobronchomalacia Tracheal stenosis Subglottic stenosis Tracheal thickening These can cause OSA, post obstructive PNA
969
Contraindications & complications for:
Thoracentesis Chest tube insertion Bronchoscopy Transbronchial biopsies Surgical lung biopsies
970
Management of anticoagulation
Warfarin x 5 days, INR <1.5 DOAC 24-48 hours LMWH x 24 hours, 6 hours if DVTp Plavix , prasugrel x 5-7? days Ticagrelor x 7 days Dipyridamol x 24 hours Platelet count >50K
971
In what conditions is bridging required?
972
Complications of suction
Increased RPO Increased pneumothorax Increased hemothorax Increased pain
973
Causes of hypoxemia post thoracentesis
RPO Pneumothorax Hemothorax V/Q mismatch immediately post
974
Risk factors for RPO following thoracentesis
Age <40 Large volume removed >1.5L ( GRAVITAS study says no) Pressure <-20 cm H2O Duration of collapse >72 hours Size of pneumothorax Diabetes
975
Indications for large bore chest tube insertion
Pneumothorax not responding to chest tube Pneumothorax on mechanical ventilation Trauma patient Hemothorax Required for talc pleurodesis
976
Microorganisms may not be pathogenic on BAL
NTM Aspergillus Candida Cryptococcus CMV, HSV
977
Microorganisms are always pathogenic on BAL
Legionella Endemic fungi Tuberculosis PJP Influenza, RSV
978
Diagnoses can be made with TBBx
Sarcoidosis Hypersensitivity pneumonitis Pneumoconiosis Lymphangitic carcinomatosis Tuberculosis CMV pneumonitis Lung transplant rejection
979
Maximum dose of lidocaine that should be used during bronchoscopy
5 mL/kg without epinephrine 7 mg/kg with epinephrine
980
Respiratory changes that occur during pregnancy
No change: VC, RR, lung compliance, resistance Increase: MV, tidal volume, VO2 max, PaO2 Decrease: TLC, FRC, ERV, RV, total respiratory compliance, PaCO2
981
What is the difference on PFTs between Pregnancy and Obesity?
In pregnancy RV will be decreased and will be increased/same in obesity
982
Cardiovascular changes that occur during pregnancy
SVR decreases, PVR decreases - BP decreases SV increases, HR increases, CO increases Increased blood volume
983
Acceptable upper limit in pregnancy for radiation
<50 milligrays or <50 mSv <5 rad
984
DDX for dyspnea in pregnancy
Physiological dyspnea in pregnancy Peripartum cardiomyopathy Tocolytic pulmonary edema Asthma Pulmonary embolism Amniotic fluid embolism Venous air embolism PAVM growth Obstructive sleep apnea
985
PE/DVT treatment in pregnancy
LMWH Warfarin and DOAC contraindicated At least 3 months + 6 weeks postpartum
986
Antibiotics that are contraindicated in pregnancy
Fluoroquinolones Aminoglycosides Septra, sulfa drugs Tetracyclines
987
Changes that occur at high altitude
Hyperventilation Increased HR and CO Hypoxic vasoconstriction Renal compensation, bicarbonate secretion Polycythemia Muscle changes - increase vascularity, increase myoglobin concentration, decrease in muscle fiber size 2,3 DPG shifts the oxygen curve RV hypertrophy Blunted response to acute hypoxemia
988
Associated complications with high altitude
Acute mountain sickness High altitude pulmonary edema High altitude cerebral edema Periodic breathing of altitude
989
Methods of assessing hypoxia at altitude
Normobaric hypoxic challenge Hypobaric hypoxic challenge Predictive equations Walk test and SpO2 Hypoxic Challenge test
990
Indications for a HAST test (High altitude Simulation Test)Hypoxic challenge Test
The obstructive algorithm, if at risk for hypercapnia The restrictive algorithm, if either PaO2 <70 OR TLC <50% CF FEV1<50% predicted Severe asthma NMD or chest wall weakness FVC <1L Baseline hypercapnia or risk of hypercapnia
991
Who does not require a HCT (Hypoxic challenge Test) BTS 2022
Stable disease previously underwent an HCT without exacerbation/change in treatment COPD with baseline SpO2 >95% and EITHER * MRC 1-2 * Desat to no less than 84% during 6MWT or SWT Previous intolerance to air travel/have had an inflight emergency (should have 2L/min provided as long as no hypercapnia Preterm infants as they should have 1-2 L prn
992
Indications for HCT (Hypoxic challenge Test) BTS 2022
COPD with resing SpO2 <95%, MRC score 3 or greater, or desat <84% on 6MWT or SWT and hypercapnia Infants with neonatal resp problems Severe asthma with persistent symptoms ILD with SpO2 <95% on exercise or PaO2 <9.42kPa or whose TLCO is <50%. Severe respiratory muscle weakness or chest wall deformity in whom FVC<1L Hypercapnia and at risk of hypercapnia including on meds that are high risk Anyone with type 2 resp failure on home O2.
993
Obstructive Lung Disease HCT Testing.
994
Restrictive lung disease HCT testing
Note kPa of 9.42 is ~ 70mmHg.
995
What is a hypoxic challenge test and possible outcomes?
Inspire 15% oxygen (estimate 8000 feet) for 20 min checking sats or ABG ABG pO2 falls below 50 or O2sat <85%
996
When is flying not recommended based on the HAST test?
pH falls <7.35 pCO2 increases by 7.5from baseline (1kPa)
997
How soon after EBUS/Pneumothorax/PE should you fly?
If a procedure was done (EBUS, TBBx, etc) * Always get opinion from interventionist. * Wait 1 week post procedure or if pneumo 1 week post resolution on CT * Note limited evidence but apparently trapped lungs are fine to travel with. If PE/DVT * Wait 2 weeks after diagnosis
998
Flying with PH
NYHA WHO class 3 or 4 should have O2 (2L/min if no hypercapnia) If on O2 should double it for the flight if no hypercapnia.
999
Contraindication to flying?
Untreated pneumothorax or not out of time frame Untreated respiratory failure Active infection with risk to others w.g. COVID, TB Bronchogenic cysts (Can cause cerebral air embolism after rupture) Type 2 respiratory failure Baseline O2 >4L (old, not really anymore?)
1000
DDX of symptoms during descent
Barotrauma of descent Nitrogen narcosis Immersion pulmonary edema
1001
DDX of symptoms during ascent
Barotrauma of ascent Decompression sickness Arterial air embolism
1002
Mechanism of barotrauma on descent vs ascent
Descent - lung squeeze below RV, pulmonary edema and hemorrhage Ascent - overinflation and possible rupture (have to exhale) → PNTX, pneumomediastinum, subcutaneous emphysema, air embolism
1003
Complications of barotrauma
Non cardiogenic pulmonary edema PNTX Pneumomediastinum Arterial gas embolism Ear trauma Sinus barotrauma Dental barotrauma
1004
Timeline of symptoms of decompression sickness
Upon surfacing Can be delayed up to 24 hours
1005
Risk factors for decompression sickness
Ascension to fast Time of dive Depth of dive (rare <10 m ) Air travel and altitude within 12 hours Right to left shunt
1006
DDx of complications while surfacing
Decompression sickness Barotrauma of ascent - expanding pneumothorax or pneumomediastinum Shallow water blackout(hyperventilation lowers Co2 prior to diving, during breath hold O2 drops, because Co2 is rising but starting at a lower point it never reaches a threshold to cause an inspiration and person loses consciousness seconcdary to hypoxemia, then person draws a breath breathing in water and drowning)
1007
Diagnostic criteria of EIB
Reduction in FEV1 by >/10% within 30 minutes of exercise Can use cycle ergometer or treadmill
1008
Indications for EIB
Diagnosis of EIB Assessment of management Assessing fitness for scuba diving
1009
Contraindications for EIB
FEV1 <75% predicted Stroke or MI in the last 3 months Uncontrolled hypertension Aortic aneurysm Recent eye surgery or ICP elevation risk
1010
Procedure for EIB
2-4 mins ramp up → rapid needed, otherwise dampens response 4-6 mins at exercise target 60% MVV (preferred), 80-90% maximum HR
1011
Causes of a false negative EIB
Exercise in last 4 hours Took asthma medications Took antihistamines in last 48 hours Warm up too long, didn’t reach in 4 mins Exercised for too long Didn’t reach max exercise
1012
Management of EIB
Treatment:SABA Prevention: SABA before exercise, +/- mast cell stabilizing agent and SAMA If using above daily or more: Controller therapy: 1) Daily ICS +/- 2) LABA, 3) LTRA
1013
Samter’s triad
Chronic rhinosinusitis with nasal polyposis Asthma NSAID/ASA intolerance
1014
Pathogenesis of AERD
NSAIDs that preferentially block COX-1 enzyme Arachidonic acid metabolized through lipoxygenase pathway Increased leukotrienes, cause bronchoconstriction
1015
Management of AERD
Maintenance ICS Add on LTRA Nasal polyp surgery, intranasal steroids ASA desensitization Dupilumab
1016
Indications for ASA desensitization in AERD
NSAID for another disease Recurrent nasal polyps recurring after surgery
1017
Risk factors for development of asthma
Personal history of atopy Family history of asthma Low birth weight, premature , IUGR Maternal smoking Pollution exposure - vehicle emissions, industrial waste Allergen exposure - dust mites, mold, cockroaches, pet dander, mice LTRIs
1018
Roles of the different TH2 mediators
IL-5: maturation of eosinophils IL-4: IgE production by cells IL-13: mucous production, hyperresponsiveness, eos recruitment IgE: mast cell degranulation TSLP: downstream signaling
1019
Symptoms that support a diagnosis of asthma
Variable symptoms and intensity Worse at night, upon awakening or after viral infections Often triggered by exercise, allergens, cold air or laughing
1020
Severity of methacholine response
1021
Contra-indications to methacholine challenge test?
Relative: * Pregnancy and nursing mothers. No studies on association with fetal abnormalities/reproductive capacity and no known whether it is excreted in breast milk. * Current use of cholinesterase inhibitor medication (for MG or PD)
1022
Definition of Asthma severity CTS 2021.
1023
Difference between difficult to treat asthma and Severe Asthma.
* Difficult to treat Asthma: * Uncontrolled Symptoms and or exacerbations despite medium or high dose ICS/LABA or maintenance OCS. May still be issues with inhaler technique, poor adherence, smoking or comorbidities, or improper diagnosis * Severe Asthma: * Uncontrolled despite adherence with maximal optimized high dose ICS/LABA and all contributing factors or if high dose treatment is decreased.
1024
When to hold medication prior to methacholine challenge.
1025
Comorbidities that should be assessed for at every visit in Asthma
Elevated BMI OSA GERD Rhinosinusitis, post nasal drip Anxiety, depression
1026
Asthma control criteria CTS
Daytime symptoms /90% personal best PEF variability <10-15% Sputum eosinophils <2-3%
1027
Severity of asthma exacerbations
Mild: just change in bronchodilators Severe: Systemic steroids, ED or hospitalization required Near fatal: required ICU, mechanical ventilation, respiratory acidosis
1028
Risk factors for severe asthma exacerbation
Current smoker (studies on tobacco, but others considered) SABA use >2 canisters/year Hx of severe exacerbation Poorly controlled FEV1 <70% Older age Female Elevated BMi Depression, anxiety Others as per GINA: comorbidities (GERD, OSA etc), elevated blood eos
1029
Risk factors for near fatal asthma exacerbation
History of near fatal asthma History of severe asthma Hx recurrent ED or hospitalizations in the last year Non adherence Missed appointments Depression, anxiety Substance use Elevated BMI
1030
Management options and their benefits in Asthma
Action plan - exacerbations Inhaled steroids - symptoms/QOL, lung function, exacerbation, mortality LABA - symptoms, lung function, exacerbation, need for reliever LAMA - lung function, exacerbation (but increased if monotherapy) LTRA - symptoms, lung function, exacerbation, need for reliever Azithromycin - symptoms, exacerbations Biologics Bronchial thermoplasty - exacerbations (increased in first 3 months), not sx or fxn Oral steroids
1031
Dose and appropriate phenotype for azithromycin therapy in Asthma
500 mg oral 3/week Inflammatory phenotype does not predict response
1032
Indications/requirements for bronchial thermoplasty
Poor control despite max medical therapy FEV1 > /60% Non smoker >/1 year No hx life threatening exacerbation <3 hospitalization in last 12 months
1033
Complications of bronchial thermoplasty
Increase exacerbation x 3 months Atelectasis Pneumonia
1034
Benefits of aerochambers
Reduce oropharyngeal deposition and side effects Improve pulmonary deposition and benefits Make actuation coordination easier
1035
Rating severity of asthma
Severe = high dose steroids + second controller OR oral steroids for >/50% of the year to keep asthma controlled or uncontrolled despite this
1036
Definition of uncontrolled asthma - One of:
Poor control - control criteria, or ACQ >/1.5 Frequent exacerbations (>/2 per year) requiring OCS (>/3 days) Serious exacerbations (>/1 per year) requiring hospitalizations, ICU, MV in the last year Airflow limitation <80% personal best
1037
Etiology of uncontrolled asthma
Non adherence Inhalation technique Exposures Comorbidities e.g. GERD, OSA, PND, etc. Alternative diagnosis Severe asthma
1038
Investigation of severe asthma
Rhinosinusitis - tx, CT sinus, ENT referral GERD - 24 hour PH monitoring OSA - PSG Psychiatric - referral EGPA - ANCA ABPA - IgE, RAST, eos VCD - ENT Bronchiectasis - CT chest, CF testing, IGAM, sputum culture
1039
Biomarkers in TH2 inflammation and their cut offs
FENO >/25 ppb Sputum eosinophils >2% Serum eosinophils >/150 Asthma allergen driven clinically
1040
Role of FENO?
Etiology of respiratory symptoms -?inflammatory Predict response to steroids or inhaled steroids Monitor response Guide management - step up, step down Evaluate adherence
1041
What is considered a significant increase or decrease in FENO?
Baseline over 50 ppb: >20% increase, >20% decrease Baseline less than 50 ppb: >10 ppb increase, >10 ppb decrease
1042
Causes of increased FENO
Atopic asthma Atopy, allergic rhinitis, eczema Eosinophilic bronchitis COPD with mixed inflammatory phenotype Viral infections Acute/chronic rejection of lung including BO
1043
Causes of decreased FENO
Smokers LTRA Rhinosinusitis Non eosinophilic asthma RADS VCD COPD Bronchiectasis, CF
1044
Benefits of biologic therapy in Asthma?
Improve symptoms Improve FEV1 Reduce exacerbations Reduce OCS - mainly mepo, benra, dupi; resi in post analysis, ?oma
1045
Notable side effects of biologic therapy in Asthma?
Injection site pain and reaction, nasopharyngitis, headaches Omalizumab - anaphylaxis Dupilumab - hypereosinophilia (do not give if baseline >1.5) Tezepelumab - anaphylaxis
1046
Treatment options for NONtype 2 asthma
LAMA Azithromycin Anti-TSLP Bronchial thermoplasty (paucigranulocytic asthma)
1047
When to hold medication prior to methacholine challenge.
1048
Treatment of asthma exacerbation
All → SABA, steroids Additional to consider: SAMA IV magnesium High dose ICS BPAP HFNC if cannot tolerate BPAP IV epinephrine - if anaphylaxis or angioedema component Ketamine - acts as anxiolytic Heliox if component of upper airway obstruction
1049
Steroid equivalents in asthma CTS.
1050
Diagnostic criteria for RADS(irritant induced asthma)
Consistent history (acute exposure preceding symptoms, no sx before) Airflow obstruction on PFT, non specific bronchial hyperresponsiveness Symptoms arise within 24 hours Symptoms last at least 3 months Exclusion of other causes
1051
Causative agents for irritant induced asthma
Chlorine Oxides of nitrogen Acetic acid Sulfur dioxide Isocyanates
1052
RFs for developing sensitizer induced OA
RFs for developing sensitizer induced OA Atopy Higher level of exposure More frequent exposure Cigarette smoking
1053
Causes of sensitizer induced OA
LMW: isocyanates (polyurethane worker, insulation installer, spray painter), dyes and bleaches (hairdressers), wood dust (carpenter), metal salt (metal plating) HMW: flour dust (baker), animal protein antigens e.g. murine urine (veterinarian, farmer) & shellfish (fish processing), natural rubber latex protein (HCW)
1054
Extrapulmonary symptoms of sensitizer induced OA
Rhinitis Urticaria, rash
1055
Investigations to confirm the diagnosis of occupational asthma
PEF - best validated method - variability >/20%* NSBHR - less sensitive and specific - > 3.2 fold* (NON-SPECIFIC BRONCHIAL HYPERRESPONSIVENESS) Specific inhalation challenge test - FEV1 drop by >/15%* Sputum eosinophils - increase by >1-2% Spirometry - less sensitive and specific
1056
Once occupational asthma is confirmed, how do we find out the causative agent?
IgE like RAST testing Specific inhalation challenge test
1057
Stages of change for smoking cessation
Pre contemplative Contemplative Preparation Action Maintenance
1058
5A’s of smoking cessation
Assess Advise Ask Assist Arrange
1059
Side effects of smoking cessation
Change in mood Weight gain Increased sputum production
1060
Benefits of smoking cessation
Rate of FEV1 decline normalizes Normal MI risk by 1 year ½ cancer risk by 10 years ½ risk of dying in next 15 years
1061
Impact of smoking on fetus
IUGR Premature birth Low birth weight SIDS Bronchopulmonary dysplasia
1062
Success rate of quitting with and without aid cessation
5% without 30% with
1063
Side effects of cessation aids
NRT: Nausea, vomiting, diarrhea, insomnia, vivid dreams, local irritation, hypersensitivity Varenicline: nausea, vomiting, diarrhea, bizarre dreams, sleep walking, insomnia Bupropion: decreased seizure threshold, suicidal or homicidal ideation, psychosis, mania or hypomania
1064
Contraindications of the cessation aids
NRT: recent ACS or stroke (<2 weeks), uncontrolled BP Varenicline: kidney disease, hypersensitivity Bupropion: <18 (suicidality), seizure disorder, AN/BN, on MAOI, on wellbutrin, hypersensitivity, discontinuation of BZD, alcohol (things that lower seizure threshold)
1065
RF for COPD development
Men Cigarette smoking (in utero, passive, active), cannabis, vaping Air pollution, biomass fuel burning Occupational exposures e.g. coal, pesticides HIV, childhood infections Genetics e.g SERPINA Early life lung insults, low birth weight
1066
Comorbidities that are associated with COPD
Lung cancer Cardiovascular disease Skeletal muscle dysfunction Osteoporosis Anxiety, depression
1067
JAMA physical examination findings with the highest LRs for COPD
Wheezing Barrel chest Decreased cardiac dullness
1068
Physiological causes of exercise limitation in COPD
Hypoxemia - V/Q mismatch Hypercapnia - DH, reached MVV Increased WOB - due to mechanics Muscle deconditioning Cardiac deconditioning, decreased preload for DH
1069
Measures of exercise tolerance?
6MWT ISWT, ESWT CPET
1070
Measures of health status
CRQ Chronic Respiratory Disease Questionnaire) Evaluated physical functional and emotional CAT SGRQ (St. George Respiratory Questionnaire) CCQ (Clinical COPD Questionnaire)
1071
Prognostic factors in COPD
BMI
1072
What can the BODE score be used to?
Referral and listing for transplant Predictor of mortality
1073
Survival associated with BODE scores (4 year survival) and its components
BMI: Obstruction (FEV1): Dyspnea (mMRC) Exertion Capacity (6MWT) 0-2: 80% 3-4: 70% 5-6: 60% 7-10: 20%
1074
Recommended vaccinations for patients with COPD
Influenza annually Pneumococcal COVID-19 as per public health Pertussis if have not had in adulthood Shingles >/50 RSV (If >60 OR chronic lung/cardiac condition)
1075
What do we use to determine treatment in COPD?per CTS VS. GOLD
mMRC <2 CAT <10 FEV1>/80% predicted Risk of future exacerbations (CTS: High Risk of AECOPD” if ≥ 2 moderate AECOPD or ≥ 1 severe exacerbation in the last year (severe AECOPD is an event requiring hospitalization or ED visit))
1076
How is the risk of AECOPD determined?
Low: /2 moderate exacerbations in the last year, >/1 severe
1077
What is moderate vs severe exacerbation in COPD?
Mild: only change in short acting bronchodilators Moderate: required steroids or abx Severe: required ED visit or hospitalization
1078
Benefits of inhaler therapies
Improve dyspnea Improve health status Improve exercise tolerance +/- Reduce risk of exacerbation +/- improve mortality
1079
When is stepping down COPD bronchodilators NOT appropriate?
Moderate-high symptom burden High risk of exacerbation Eos >300
1080
Indications that strongly favour ICS (as per GOLD)
>/2 moderate exacerbations for AECOPD ED visit or hospitalization for AECOPD History of concomitant asthma Blood eosinophils >/300
1081
ICS not strongly favoured (as per GOLD)
Eosinophils <100 Recurrent pneumonias Hx of NTM disease
1082
Indications for oral therapies in COPD
Symptomatic, high risk AECOPD group Exacerbate despite triple therapy + chronic bronchitis phenotype for 2 of them
1083
Benefits of oral therapies in COPD
Decrease exacerbation
1084
Treatments that improve exercise tolerance in COPD
Smoking cessation Appropriate bronchodilators Pulmonary rehabilitation Supplemental O2 in those who qualify LVRS in appropriate patients Bullectomy in certain patients Endoscopic procedures Lung transplantation
1085
Treatments that reduce the risk of exacerbation in COPD
Appropriate bronchodilators - dual and triple Oral therapies as indicated Case management AND education Pulmonary rehabilitation within 4 weeks of AECOPD Smoking cessation Influenza vaccination
1086
Treatments that reduce mortality in COPD
Smoking cessation Triple therapy (SITT) PR within 4 weeks of AECOPD O2 in resting hypoxemia( PaO2 <55 or <60 with core pulmonale/evidence of elevated hgb) NIV acutely, or chronic hypercapnia LVRS in appropriate patients ?Transplant in some
1087
Ways to manage dyspnea in COPD (CTS table)
Walking aids Pursed lip breathing Neuromuscular electrical muscle stimulation Low dose opioids Oxygen in resting hypoxemia
1088
Possible intervention in the treatment of COPD
LVRS Bullectomy Endoscopic procedures Lung transplant
1089
Who would be eligible for LVRS?
Symptomatic from emphysema and not CB/asthma Smoking cessation >4 months Heterogeneous emphysema Upper lobe predominant emphysema TLC >/100% RV >/150% FEV 140 m
1090
What are the contraindications to LVRS?
Comorbid disease with life expectancy <2 years Severe CAD or other cardiac disorder BMI >31 FEV1 ⅓ chest Extensive pleural symphysis e.g. previous infection, pleurodesis O2 >6L/min PaCO2 >60 mmHg or PaO2 <45 on room air PAP >/35 mmHg Prednisone >20 mg oral daily
1091
Benefits of LVRS
Dyspnea HRQOL Exercise tolerance Lung function Mortality in some → upper lobe emphysema, low baseline exercise tolerance
1092
Indications for treatment of giant bullae
Symptomatic Complications >/30% of hemithorax
1093
Risk factors for COPDE
Older age Low FEV1 at baseline Previous COPD exacerbations ** Eos >/300 ** Chronic mucous hypersecretion Duration of COPD Pulmonary HTN GERD
1094
Treatment of AECOPD
SABA, SAMA Steroids 40 mg oral daily x 5 days - hasten recovery, reduce relapse, improve FEV1 Antibiotics if meet criteria - hasten recovery, reduce relapse IV magnesium
1095
Abx options for treatment AECOPD
Amoxi-clav Fluoroquinolones Macrolides Tetracyclines e.g. doxycycline
1096
Indications for NIV in AECOPD?
pH <7.35, PcO2 >/45 Worsening WOB Persistent and refractory hypoxemia
1097
Different allele variants in A1AT deficiency
Normal - M Deficient - Z/S Dysfunctional - F Null
1098
Genotypes that have the highest risk of A1AT (in order)
-/- (least common) Z/Z Z/S (if they smoke) Z/M (if they smoke)
1099
Indications to screen for A1AT
Age <65 OR Pack year <20
1100
Non pulmonary manifestations of A1AT
Transaminitis Cirrhosis HCC Necrotizing panniculitis GPA/ANCA vasculitis Intracranial aneurysms Fibromuscular dysplasia
1101
Diagnosis of A1AT
Applicable genotype A1AT level <11 mmol/L or 57 mg/dL (our units)
1102
Indications for treatment of A1AT
AAT <11 umol/L or 57 mg/dL (our units) FEV1 25-80% On maximal pharmacological and non pharm therapy (including PR) Have quit smoking - non-smokers or ex-smokers (nothing in guidelines, funding requires at least 6 months)
1103
Benefits of augmentation therapy in A1AT
Improve lung density on CT Improve FEV1 Improve mortality
1104
Benefits of supplemental O2 therapy at rest in COPD
Mortality benefit in those that qualify Improved dyspnea Improved exercise tolerance Improved physiological effect e.g. ?decreased PH
1105
Benefits of supplemental therapy with ambulation in COPD
Improved HRQOL Improved outdoor mobility Not clear re: dyspnea, exercise capacity
1106
3 types of patients with COPD that would benefit from O2
Resting hypoxemia Resting hypoxemia and comorbidities listed Patient planning for air travel if they meet criteria ?Ambulatory or exertional hypoxemia
1107
Duration of PR programs
Minimum 8 weeks Minimum 24 sessions, 16 should be supervised
1108
Quality indicators of a PR program
Necessary HCP, and resources: Cycle ergometer, treadmill, flat open space Vital machines Education material Etc. Baseline intake indicators: Dyspnea Health status Exercise capacity 1 Repetition maximum Aerobic exercise prescription Strength training prescription Exercise indicators Monitoring indicators Education and self management component Post program
1109
4 parameters that are needed for exercise prescription (aerobic)
Frequency - 3 sessions Intensity - 60% VO2 max Time - 20 mins each session Type - aerobic - treadmill, free walking, stair climb, ergometer (NOT arm alone)
1110
4 parameters that are needed for exercise prescription (strength)
Frequency - 2-3 times per week Intensity - 60% of 1-RM Time - 1-3 sets, 8-12 repetitions each Type - weights, resistance bands
1111
Minimum health outcomes that need to be measured before and after PR
Aerobic exercise endurance Muscle function Health status Others case by case: psychological status, nutrition status, self efficacy, etc.
1112
Indications for referral to PR
COPD - regardless of FEV1 or smoking status ILD PHTN
1113
Proven benefits of PR
COPD - dyspnea, HRQOL, exercise capacity, social/physical fxn, reduce anxiety, depression, ??mortality ILD - dyspnea, HRQOL, exercise capacity PHTN - dyspnea, HRQOL, exercise capacity
1114
Physiological benefits post PR for COPD
Improved VO2 max Improved O2 pulse Decrease in HR Increased AT Increased muscle mass Decrease dynamic hyperinflation
1115
Which post COVID patients are appropriate for PR referral?
New respiratory symptoms post COVID + At least 1 of: new O2 requirements, persistent reticular/fibrotic changes on imaging, new and persistent restriction/obstruction/DLCO impairment on PFTs
1116
Causes of eosinophilic lung diseases
Acute/chronic eosinophilic pneumonia EGPA HES ABPA Infections - parasites, fungal Neoplastic - e.g. paraneoplastic PLCH Lung transplantation
1117
Causes of AEP
Idiopathic Smoking - new, increased uptake, different type Inhalation drugs- cocaine, marijuana Medications - daptomycin**, antidepressants Occupational exposures Infections - parasites, fungi
1118
Imaging findings in eosinophilic pneumonia
Acute: diffuse, bilateral GGO, bronchovascular thickening, effusion, LN Chronic: peripheral, bilateral GGO, upper lobe, migrating
1119
Differences between AEP and CEP
Causes - allergic/atopic causes in chronic Clinical manifestations - symptoms, timeline Relapse - common chronic Imaging Peripheral eosinophils - seen in chronic Both have elevated IgE Both have BAL eos >25% Both are treated with steroids
1120
Diagnostic criteria for AEP
Acute onset, <30 days Patchy infiltrates on CXR/CT BAL eos >25% Absence of other specific eosinophilic diseases Diagnostic criteria for CEP is similar, except that timeline is 4-5 months and imaging is peripheral infiltrates
1121
Diagnostic criteria of HES
HE + eosinophilic mediated damage + other causes excluded HE: >1.5 on 2 occasions at least 1 month apart, and >20% (2024 says 10%) on BM, and extensive eos infiltration on pathology
1122
How is surfactant produced?
Type II pneumocytes secrete surfactant Surfactant is mix of proteins + lipids (mainly phosphatidylcholine)
1123
Causes of PAP
Idiopathic Primary: Hereditary Autoimmune Secondary (HI/TII): Infections e.g. nocardia, PJP, tuberculosis Inhalation exposures e.g. silicosis, chlorine, bakery powder Transplantation e.g. SOT, HSCT Hematological malignancies e.g. MM, WM Immunodeficiencies e.g. CVID
1124
BAL findings in PAP
Cloudy Foamy macrophages Send for PAS stain on cytology → PAS+ macrophages on background of PAS material
1125
Other investigations in PAP
Anti GM CSF antibodies GM CSF serum levels GM CSF receptor function BAL TBBx - not required for biopsy
1126
Pathological findings of PAP
Normal alveolar structure Lipo Proteinaceous material fills terminal bronchioles and alveoli This material stains positive on PAS stain If done, electron microscopy shows lamellar bodies
1127
Treatment options for PAP
Inhaled GM-CSF Therapy Whole lung lavage Treat secondary cause Lung transplantation Rituximab, PLEX - case reports
1128
Indications for whole lung lavage
Definitive histological diagnosis + PaO2 <65, or A-a >/40 or severe dyspnea/hypoxia at rest or exercise
1129
Imaging findings and distribution of different cystic lung diseases
LAM = diffuse, random, small cysts BHD = lentiform, paramediastinal, peripheral, subpleural PLCH = bizarre shaped, upper lobe predominant, spare costophrenic angles, nodules/cavities LIP = diffuse, random, GGO in between Amyloid/LCDD = cysts varying sizes/shapes, nodules, cavitations, opacities lower lobes/subpleural
1130
Special pathological tests for different cystic lung diseases
LAM = HMB-45 positive smooth muscle cells PLCH = S100 and CD1 a positive langerhans cells, intracellular Birbeck granules Amyloid = apple green birefringence by congo red stain LCDD = kappa light chains lacking the above
1131
Pulmonary manifestations of PLCH
Cystic lung disease Group 5 HTN Eosinophilic lung disease
1132
Extrapulmonary manifestations of PLCH
Rash - brown papules Lytic bone lesions Central diabetes insipidus
1133
Treatment of PLCH
Smoking cessation Steroids in some Chemotherapy in some Transplantation
1134
Extrapulmonary manifestations of BHD
Fibrofolliculomas Skin tags Renal tumors
1135
Extraparenchymal manifestations of LAM
Angiofibromas Leiomyoma Angiomyolipoma Lymphadenopathy Pleural effusions Meningiomas
1136
Pathological features of LAM
Lung cysts Smooth muscle-like cell (LAM cells) infiltration of parenchyma and lymphatics Stain positive for HMB45, s.m. actin Have ER/PR receptors Express VEGFC/D
1137
Diagnostic criteria for LAM → table
1138
Differential diagnosis for cystic lung disease
1139
Indications for treatment of LAM
FVC <70% Case by case basis for those who: Resting hypoxemia PaO2 <70 Exercise induced desaturation RV >120% DLCO <80% Progression of disease (FVC loss >/90 cc per year Heavy burden of cysts >30% of lungs Chylous effusion AML >4 cm
1140
Benefits of mTOR inhibitor as per the MILES study in LAM(Sirolimus)
Improve symptoms Improve QOL Stabilize lung function Reduce VEGFD
1141
Management of complications of LAM
Pneumothorax:Pleurodesis after first episode, advised not to air travel x 1 month Chylothorax: chest tubes, consider mTOR inhibitor Angiomyolipoma: embolization, radiofrequency ablation, consider mTOR if >/4 cm
1142
Screening investigations that are required in LAM
Abdominal CT for all Brain MRI if symptoms, or increased risk (e.g progesterone) Basically looking for evidence of TSC given that is more common
1143
Secondary causes of LIP
Idiopathic Connective tissue diseases Immunodeficiency e.g. CVID Infections e.g. HIV, tuberculosis PAP
1144
PFT findings in different bronchiolar disorders
Proliferative - restrictive Obliterative - obstructive Follicular - mixed, restrictive, obstructive Diffuse panbronchiolitis - mixed, restrictive, obstructive
1145
Imaging findings of different bronchiolar disorders
Proliferative: patchy airspace, migratory, reverse halo, with distribution subpleural/peripheral, peribronchovascular Obliterative: mosaic attenuation, centrilobular nodules, gas trapping bronchial wall thickening, bronchiectasis Follicular: centrilobular nodules, tree in bud Diffuse panbronchiolitis: centrilobular nodules, tree in bud, bronchiectasis
1146
3 features of COP on CT
Distribution peripheral, subpleural, migrating, peribronchovascular, bilat GGO or consolidative alveolar opacities Atoll sign (Reverse halo sign-more common with OP and less commonly fungal but mucormycosis most common of the fungal)
1147
Diagnosis of bronchiolitis
Surgical lung bx Post transplant BOS can be clinical
1148
Pathological findings of bronchiolitis
Proliferative - intrabronchial polypoid protrusions (mason bodies) Obliterative - Lymphocytic inflammation of submucosa, in growth of fibromyxoid granulation tissue into airway, obliteration of airway - extrinsic compression of bronchioles by fibroinflammatory process Follicular: hyperplastic lymphoid tissue along bronchial walls that obliterate lumen Diffuse panbronchiolitis: lymphoplasmacytic inflammation of bronchioles; infiltration with lipid laden foamy macrophages, lymphocytes, plasma cells
1149
Causes of proliferative bronchiolitis/organizing pneumonia
Idiopathic Immune deficiency Inhalational injury Infections e.g. COVID Malignancy, chemotherapy, radiation CTD Medications Aspiration Post transplantation
1150
Causes of obliterative bronchiolitis
Post allograft transplantation (HSCT, lung) Inhalational injury e.g. silo, sulfur, silica, diacetyl Infection CTD, especially RA
1151
Causes of follicular bronchiolitis
Idiopathic CTD, especially Sjogren’s; RA, SLE Infection e.g. TB, HIV Immunodeficiency Chronic inflammatory e.g. bronchiectasis, CF, asthma
1152
Causes of diffuse panbronchiolitis
CTD e.g. RA Ulcerative colitis Lymphoma Basically always nonsmokers in Japanese and Korean patients
1153
Treatment of the bronchiolar disorders
Proliferative: steroids Obliterative: depends on cause Follicular: steroids Diffuse panbronchiolitis: erythromycin, bronchodilators
1154
Treatment of COP if not responding to steroids
Azathioprine MMF Obviously treat underlying cause
1155
Pulmonary manifestations of immunodeficiency
GLILD LIP Follicular bronchiolitis Bronchiectasis Organizing pneumonia PAP Recurrent pneumonias
1156
Non pulmonary manifestations of immunodeficiency
Granulomas in other organs Non hodgkin’s lymphoma Pernicious anemia Thyroiditis
1157
Imaging findings of GLILD
Hilar and mediastinal LN Bronchiectasis GG and solid nodular opacities
1158
Malignancies at highest risk for Radiation Induced Lung Disease
Lung cancer Mediastinal lymphoma Breast cancer
1159
RFs for development of radiation pneumonitis
Dose of radiation (usually >40, very rare <20) Volume of lung irradiated (V20 >/30%) Form of radiation e.g. SBRT lower risk Fraction of radiation Previous chemotherapy Underlying lung disease e.g. ILD**, COPD Concomitant chemotherapy Female > male Smoker Older age
1160
Phases of development of radiation pneumonitis
Initial = increased capillary permeability Latent = increased goblet cells Acute exudative = radiation pneumonitis = 1-3 months = epithelial cell sloughing, microvascular thrombosis, alveolar exudate and hyaline membranes Intermediate = 3-6 months = resolution of hyaline membranes Fibrosis = >6 months = fibrosis
1161
Time line of radiation induced lung disease
Radiation pneumonitis - within 1-3 months Radiation fibrosis - 6-12 months Radiation recall pneumonitis - really anytime * Pneumonitis in the same radiation field. Usually triggered by systemic treatment or infection.
1162
Symptoms of radiation pneumonitis
Fever, malaise, weight loss Dyspnea Dry cough Pleuritic chest pain
1163
Imaging findings in radiation pneumonitis
GGO Consolidation Straight line pattern, radiation port edges Small pleural effusion
1164
Pathological findings of radiation pneumonitis
Epithelial and endothelial cell sloughing Fibrin rich alveolar exudate Hyaline membrane formation Microvascular thrombosis
1165
Lung diseases are associated with smoking
DIP RB ILD PLCH
1166
Lung diseases that have smoking as a risk factor
IPAF RA ILD
1167
Lung diseases are actually less common in smokers
Sarcoidosis HP
1168
Other than smoking, causes of DIP
Idiopathic Occupational exposures e.g. metal worker Drug reactions Autoimmune conditions
1169
Imaging differences RB-ILD vs DIP
RB-ILD: centrilobular GGO nodules, upper lobe predominant, preserved lung volumes DIP: GGO, +/- cysts, reticular opacities, lower lobe predominance
1170
BAL findings RBILD vs DIP
RB-ILD: pigmented macrophages, unlikely to have other cells DIP: pigmented macrophages, may have increased lymphs/eos/neuts
1171
PFT RBILD vs DIP
RB-ILD: can be obstructive, restrictive or mixed DIP: usually restrictive
1172
Exogenous causes of lipoid pneumonia
E cigarettes Mineral based laxatives Petroleum jelly lubricants (used in tracheostomy care) Nasal decongestants Fire eaters
1173
Endogenous causes of lipoid pneumonia
Bronchial obstruction PAP Lipid storage and metabolism disorders Chronic inflammatory disorders e.g. CTD
1174
Imaging findings of lipoid pneumonia
GGO or consolidation Crazy paving pattern
1175
BAL features of lipoid pneumonia
Lipid laden macrophages Are detected by oil red O staining
1176
Red flags for cough
Age - > 55 years old Smoker, ex smoker Hemoptysis Dysphonia, dysphagia Recurrent pneumonia Prominent dyspnea Systemic symptoms Vomiting
1177
How does albuterol cause lactic acidosis?
Type A lactic acidosis - hypoxic or hypoperfusion Type B lactic acidosis - malignancies, drugs and inborn errors of metabolism Albuterol, by creating hyperadrenergic state enhances glycogenolysis and gluconeogenesis, leading to more glucose, pyruvate production. Lipolysis and increased FFA inhibit pyruvate dehydrogenase enzyme, so it doesn’t enter krebs cycle and is reduced to lactate
1178
Absolute and relative contraindications to cardiopulmonary exercise testing
1179
How would you predict the maximal HR for a CPET according to ERS? (M and F)
Male MaxHR =207-0.78(Age) Female Max Hr=209-0.86(Age)
1180
Indications for cessation of exercise termination in a CPET (ATS)
1181
What defines a maximal test according to ERS 2019
1182
What defines an abnormal exercise response ERS 2019 on CPET.
1183
What is the cause of limitation based on ERS 2019 on CPETs?
1184
What is the cause of limitation based on ATS on CPETs?
1185
What are the four phases of general CPET protocols based on ERS 2019.
1186
Difference on CPET between cycling and Treadmill (ATS2001)
1187
Difference between fibrosing mediastinitis and mediastinal granuloma?
1188
What is the triad of hepatopulmonary syndrome
Liver disease Intrapulmonary vasodilation Gas exchange abnormalities
1189
Define and write the equation for oxygen content (CaO2)
Oxygen content — The arterial oxygen content (CaO2) is the amount of oxygen bound to hemoglobin plus the amount of oxygen dissolved in arterial blood: CaO2 (mL O2/dL) = (1.34 x hemoglobin concentration x SaO2) + (0.0031 x PaO2) where SaO2 is the arterial oxyhemoglobin saturation and PaO2 is the arterial oxygen tension
1190
Define and write the equation for oxygen delivery (DO2)
Oxygen delivery — Oxygen delivery (DO2) is the rate at which oxygen is transported from the lungs to the microcirculation: DO2 (mL/min) = Q x CaO2 where Q is the cardiac output.
1191
Define and write the equation for oxygen consumption(VO2)
Oxygen consumption — Oxygen consumption (VO2) is the rate at which oxygen is removed from the blood for use by the tissues. It can be measured directly or calculated. Both approaches assume that all unused oxygen passes from the arterial to the venous circulation. VO2 (mL O2/min) = Q x (CaO2 - CvO2)
1192
What are important bacteria for those with reduced cell counts?
<200: PJP, endemic fungi, aspergillus, candida <100: Toxoplasmosis <50: MAC, CMV
1193
Causes of pulmonary disease in HIV?
ILD - OP, NSIP, LIP PAP Emphysema Bronchiectasis Bronchiolitis - obliterative, follicular Pulmonary hypertension HIV Cardiomyopathy causing pulmonary edema Drug reaction to HAART or other medications Various infections Various malignancies
1194
Manifestations of kaposi sarcoma
Skin disease Parenchymal disease Endobronchial disease Mediastinal lymphadenopathy
1195
Imaging findings in Kaposi Sarcoma
Flame shaped, ill defined opacities Interlobular septal thickening Lymphadenopathy
1196
Publicly reported illnesses
Legionella Invasive pneumococcal disease Influenza H. influenza HIV Tuberculosis SARS COVID Legally, I have to share COVID-19 news
1197
Most common bacterial causes of CAP
Strep Staph H influenza Mycoplasma Atypicals Aerobic gram negative → klebsiella, e. Coli, enterobacter, pseudomonas, serratia, proteus, acintobacter Anaerobes
1198
Most common causes of VAP
Strep Staph - MSSA and MRSA ** Pseudomonas ** Gram negative bacilli
1199
Bacterial causes of cavitary pneumonia
Klebsiella Staphylococcus Anaerobes Nocardia Actinomyces Rhodococcus TB/NTM Endemic fungi
1200
Organisms that cause interstitial infiltrates
Legionella Mycoplasma Chlamydia Viruses
1201
Imaging features of viral pneumonia
Interstitial infiltrates - can be reticular, reticulonodular Miliary pattern Airspace opacities or consolidation Peribronchial thickening
1202
When is 5 days of antibiotic treatment OK vs. 10 days?
Afebrile x 48 hours AND 100, BP <90, RR>24, SpO2 <90%, normal mental status
1203
Complications of MSSA pneumonia
Abscess Cavitation Pleural effusion Bacteremia Resistance to MRSA
1204
Risk factors for VAP
Paralysis Head injury or unconscious Aspiration Chronic lung disease Nasogastric tubes Condensate in ventilator tubing Supine position
1205
Diagnostic criteria for VAP
Occur >/48 hours of intubation Not present before intubation/wasn’t the reason for intubation New or progressive infiltrates on imaging Clinical evidence of infection e.g. fever, purulent sputum, leukocytosis, hypoxemia Positive pathogen required by some definitions
1206
Methods to diagnose causative agent in VAP
Invasive (BAL, brush, biopsy) > non invasive (endotracheal aspirate) Quantitative (colony forming units) > semi quantitative (1+/2+ growth rates)
1207
Measures to reduce VAP
Head of bed elevated 30-45 degrees Mouth hygiene (tooth brushing but no chlorhexidine) Enteral over parenteral nutrition Only clean tubing when there is visible soiling Limit sedation Subglottic drainage Ventilator liberation where possible Maintain physical functioning
1208
Complications of strep pneumonia
Empyema Meningitis Endocarditis Pericarditis Septic arthritis Invasive streptococcal disease - CSF, blood, pleural, pericardial, synovial
1209
RFs for IPD
Age Chronic heart disease Chronic lung disease e.g. asthma requiring medical care in last year Chronic liver disease Chronic kidney disease Diabetes Malnutrition Immunodeficiency Splenectomy, functional asplenia from sickle cell HIV infection HSC transplant SOT transplant Leukemia and lymphoma Immunosuppressive therapy
1210
Risk factors for drug resistant strep pneumo
>65 or <2 Daycare or institutional setting (exposure to child) Beta lactam use within 3-6 months Medical comorbidities Immunocompromised EtOH
1211
Indications to test for legionella
Severe CAP Not responding to beta lactam Epidemiological factors e.g. outbreak
1212
Diagnostic test for legionella
Urine legionella antigen PCR Culture
1213
Treatment regimen for legionella
Azithromycin 500 or levofloxacin 750 Duration: 7 days (mild), 10 days (severe), 14 days (immunocompromised)
1214
Viral causes of pneumonia
COVID-19 Influenza A and B RSV Parainfluenza Rhinovirus Adenovirus
1215
RFs for a more severe response to influenza
>/65 years old Pregnant Postpartum up to 2 weeks Long term care, nursing homes Chronic medical condition - respiratory, renal, liver, etc. Immunosuppression
1216
The common superinfections post influenza
Staph aureus Streptococcus
1217
Diagnostic options for influenza and COVID
Rapid antigen test RT-PCR Cultures
1218
Benefits of oseltamivir
Reduce duration of symptoms Reduce risk of death in inpatients Within 48 hours has best outcomes
1219
COVID-19 imaging findings
GGO Consolidation Crazy paving Bronchovascular thickening Pleural effusion, LN
1220
Current COVID-19 therapies
Mild: budesonide, remdesivir, Paxlovid, fluvoxamine Moderate: dexamethasone, remdesivir, tocilizumab, baricitinib Severe: dexamethasone, tocilizumab, baricitinib
1221
COVID-19 vaccines available
MRNA - pericarditis, myocarditis, Bell’s palsy, anaphylaxis Vector - VTE, GBS, anaphylaxis
1222
Treatment of echinococcal cyst
Antiparasitic therapy e.g. albendazole Consider surgical resection Consider percutaneous aspiration