APCCMPD Chapters Flashcards
Define chronic bronchitis
Chronic bronchitis- 3+ months of cough in a year for 2 consecutive years, other causes of cough ruled out
Define emphysema
Emphysema- permanent destruction of airspaces (terminal bronchioles and alveoli)
Differentiate centrilobular, panacinar, and paraseptal emphysema
Depends what part of the lobule/terminal airway has damange
Centrilobular- damage/destruction of central part of acinus
-seen in smokers, coal workers pneumoconiosis
Panacinar- all parts of the acinus destroyed
-smoking, alpha-1 antitrypsin deficiency
Purpose of GOLD criteria in use clinically
GOLD- to risk stratify patients by degree of obstruction (based on FEV1) and symptoms (mMRC and CAT score) to determine treatment, also to determine risk of future exacerbation
Name LABA/LAMA combinations
LABA/LAMA
vilanterol/umeclidinum = Anoro Elipta
Olodaterol/tiotropium = Stiolto respimat
2 ways that GOLD criteria distinguishes respiratory symptoms
Classifying respiratory symptoms by
-mMRC: 0-1 scale of dyspnea
mMRC 0-1: A and C GOLD disease
mMRC 2 or above: B and D
-CAT (COPD assessment test): questions about symptoms (cough, dyspnea) cuttoff below or above 10, max is 40 (8 questions ranked 1-5, higher is worse), above 10 indicates worse disease
CAT below 10: A, C
CAT above 10: B, D GOLD disease
Scale for mMRC
mMRC: perceived dyspnea scale
0- no concerning dyspnea, breathless only with strenuous exercise
1- SOB when hurrying
2- walk slower b/c of breathlessness
3- stop to catch breath after 100m or a few minutes on level surface
4- breathlessness with ADLs (dressing), leaving house
Scale for CAT
0-40, cutoff for GOLD is under 10 (minimal) vs. over 10 (bad symptoms)
8 questions total, rank on scale of 0 (no symptoms) to 5 (severe or constant symptoms)
Differentiate GOLD 1-4 for degree of flow obstruction
GOLD by FEV1
1- over 80% predicted
2- 50-79% predicted
3- 30-49%
4- under 30% predicted
Differentiate GOLD A-D
GOLD by symptom categorization and exacerbations
GOLD A: mMRC 0-1 or CAT under 10, 0-1 moderate exacerbation a year (not leading to hospitalizations)
GOLD B: mMRC over 2 or CAT over 10, 0-1 moderate exacerbations a year (not leading to hospitalization)
GOLD C: mMRC 0-1 or CAT under 10, 2 or more moderate exacerbations or at least one leading to hospitalization
GOLD D: mMRC over 2 or CAT over 10, 2 or more moderate exacerbations or at least 1 requiring hospitalization in the past year
Differentiate treatment options delineated by GOLD Groups A-D
For GOLD A (low symptoms, low exacerbations) can try SABA alone
For Gold B and C (either low symptoms high exacerbations or high symptoms low exacerbations) try LAMA/LABA combo
Gold D- triple therapy
Guidelines for LAMA alone vs. LAMA/LABA for COPD
For COPD pts with dyspnea or exercise intolerance - combo LAMA/LABA recommended over monotherapy
from 2019 GOLD GUidelines
-combo LAMA/LABA increases FEV1, reduces symptoms, reduces exacerbations compared to monotherapy
When to escalate from LAMA/LABA to triple therapy (ICS/LAMA/LABA?)
Add ICS if have an exacerbation, requiring steroids/abx (even if managed outpatient)
COPD pts with dyspnea or exercise intolerance despite LAMA/LABA escalate to triple therapy if one or more exacerbations in the past year requiring abx or oral steroids
2019 GOLD Guidelines: inhaled triple therapy improves lung function, symptoms, and reduce exacerbations
-so once already on LABA/LAMA but don’t start on triple off the bat
65M COPD, FEV1 45%, 1 exacerbation in the past year
Best treatment plan?
GOLD class 3 (FEV 30-49%) B (1 exacerbation)- start combination LAMA/LABA (anoro, stiolto respimat)
2019 Gold Guidelines: combo better than either monotherapy
LAMA improves mortality, symptoms, and/or FEV1?
LAMA improves symptoms and quality of life
No improvement in mortality or FEV1
70F FEV1 40% on ICS/LAMA/LABA, mMRC 4, 1 exacerbation in the past year managed outpatient with antibiotics and steroids
GOLD class? (number and letter)
GOLD 3B
3 (FEV1 39-49%)
B not A b/c mMRC over 1
B not D b/c only one moderate exacerbation (would need 2 or more moderate within a year or at least one hospitalization)
Proven benefits of LAMA (vs. placebo)
UPLIFT trial- NEJM 2008
-Improved symptoms, quality of life, exacerbation, COPD admissions
NO reduction in FEV1 or mortality
TORCH trial- proven benefit of ICS/LABA
TORCH trial- NEJM 2007: ICS/LABA vs. placebo vs. either alone
-Combo ICS/LABA Improved symptoms, improved FEV1, reduced exacerbation
vs. placebo or either ICS or LABA alone
ATS Guidelines for positive PPD in the following cases
(a) 5mm or greater
(b) 10mm or greater
(c) 15mm or greater
ATS guidelines for positive PPD
(a) 5mm or greater in those w/ high risk of progression to active Tb
-HIV, TNFalpha inhibitor/immunocompromised
-those with close contact of recent positive case
-abnormal CXR c/w prior Tb infection
-silicosis
(b) 10mm or greater: those at increased risk of prior exposure or intermediate risk of progression to active
-Exposure: from endemic country (India), prison/homeless, healthcare workers
-Comorbidities that increase risk of progression: DM, CKD, IVDU
(c) 15mm or greater = everyone else
ATS Guidelines for positive PPD in the following cases
(a) TNF-alpha inhibitor
(b) IVDU
(c) From India
(d) Close contact of recent TB case
(e) Healthcare workers
(f) Prison/homeless
(g) Abnormal CXR c/w prior Tb
(h) Silicosis
(i) Chronic renal failure
ATS guidelines for positive PPD
(a) 5mm or greater in those w/ high risk of progression to active Tb
-HIV, TNFalpha inhibitor/immunocompromised
-those with close contact of recent positive case
-abnormal CXR c/w prior Tb infection
-silicosis
(b) 10mm or greater: those at increased risk of prior exposure or intermediate risk of progression to active
-Exposure: from endemic country (India), prison/homeless, healthcare workers
-Comorbidities that increase risk of progression: DM, CKD, IVDU
(c) 15mm or greater = everyone else
What patients be most concerned about a false-negative PPD?
False-negative PPD in:
-acute disease, first 6-8 weeks
-immunocompromised (truly no Ab response)
-such widespread disseminated disease (miliary)
What patients be most concerned about a false-positive PPD?
False-positive PPD:
-BCG vaccine (still given to prevent CNS Tb)
-NTM
First line tx for LTBI
LTBI: 4R
-rifampin daily x4 months
Second line alternative regimens for LTBI (aside from 4R)
LTBI regimens aside from 4R
-INH daily x6 mo
-Rifapentine + INH weekly x3 mo
-Rifampin + INH daily x3 mo
Differentiate LFT abnormality expected from rifampin vs. INH
LFT abnormality
Rifampin- expect cholestatic picture (alk phos, bilis)
INH- expect transaminitis
Which LTBI regimens to add pyridoxine to and why
B6 whenever using INH to prevent peripheral neuropathy
-if pt has tingling/symptoms increase B6 dose
Typical treatment regimen for pan-sensitive tuberculosis
IRPE + pyridoxine
-stop ethambutol if returns rifampin sensitive
-stop PZA after 2 months
-continue rifampin + INH for additional 4 months (6 months total)
Longer (9 mo) for severe cavitary disease or CNS involvement
Diagnostic criteria for MAC infection
MAC infection per ATS guidelines
Appropriate clinical picture, radiographic findings, and exclusion of other things (ex: Tb)
Micro data: 2 positive sputum Cx OR 1 + BAL OR 1 + tissue (BAL with AFB or granulomatous inflammation)
2020 Guidelines for first line treatment of nodular bronchiectatic MAC
(a) Drug regimen
(b) Duration
(a) Azithro
Rifampin
Ethambutol
-TIW can be used for most nodular bronchiectatic disease as better tolerated and shown to have similar sputum conversion rates in moderate (not severe or fibrocavitary disease)
(b) for 12 months from sputum culture conversion (test sputum each month, 12 months from conversion)
When daily MAC tx is indicated over 3x/week
-severe nodular bronchiectatic disease
-fibrocavitary disease
What is considered refractory MAC?
(a) Tx
Pts who remain culture positive at 6 months of azithro, rifampin, ethambutol
(a) Add inhaled amikacin
Have pt with MAC pending sensitivities- when to start abx?
Start azithro, rifampin, ethambutol prior to sensitivities.
Sensitivity in vitro doesn’t necessarily correlate with in vivo for rifampin and ethambutol so really waiting on azithro R and can then add another agent if needed
What monitoring needs to be done on MAC therapy?
(a) Standard first line tx for nodular bronchiectatic MAC
(b) Rifabutin
(c) Amikacin
MAC therapy monitoring
-monthly sputum culture until conversion
(a)
Azithro- QTc, LFTs
Rifampin- LFTs
Ethambutol- LFTs, visual acuity, visual color discrimination
(b) Rifabutin- LFTs, CBC (leukopenia and thrombocytopenia), visual acuity testing
(c) Amikacin- BUN/CR, audiometry
Differentiate tx regimens for M. kansasii and M. abscessus
M. kansasii = same regimen as MAC = azithro, rifampin, ethambutol
M. abscessus tx way more complicated, no idea regimen
-first depends on azithro resistance (inducible resistance with erm gene)
Macrolide sensitive: 3 drug regimen with azithro
-can add: IV amikacin, IV tigecycline
oral: azithro, clofazimine, linezolid
inhaled: amikacin
Azithro resistsance strains of M. abscessus need at elast 4 drugs above
What is an erm gene
(a) What means for cultures
Erm = erythromycin ribosome methyltransferase gene
-gene that leads to inducible macrolide resistance in Mycobacterium abscessus
(a) Need to keep cultures 14 days b/c may seem sensitive initially then develops macrolide resistance by day 14
Indications for roflumilast in COPD (REACT trial, Lancet 2015)
Chronic bronchitis (have to have cough) and at least 2 exacerbations in the previous year
-fewer exacerbations
Indications for chronic azithromycin therapy in COPD (NEJM 2011)
Moderate to severe COPD and either
-continuous O2 therapy
-or one exacerbation in the last yera
-longer time to first exacerbation
-fewer exacerbations
Differentiate pts better for roflumilast vs. chronic azithro for severe COPD
Roflumilast- in pts w/ 2 or more exacerbations in the past year and chronic bronchitis phenotype (so cough!)
vs.
Chronic azithro: on continuous O2 or at least one exacerbation
Benefit of supplemental O2 in COPD
(a) At rest
(b) On exertion
Supplemental O2
(a) For resting hypoxemia (SpO2 88 or under, PaO2 55 or under) continuous O2 therapy reduces mortality (Annals Int Med 1980, Lancet 1981)
(b) LOTT trial, NEJM 2016- no decrease in mortality or time to first hospitalization in pts with stable COPD and moderate desat at rest (89-93%) or with exercise (80-90%)
Roflumilast
(a) Mechanism of action
(b) Main side effect
Roflumilast = reduces exacerbations in pts with COPD and chronic bronchitis (chronic cough) with frequent (more than 2 in the past year) exacerbations
(a) PDE4 inhibitor- oral, thought to promote airway smooth muscle relaxation
(b) Diarrhea in 10%
Who should be referred for pulmonary rehab?
All COPD patients with severe obstruction which GOLD guidelines 2015 state as FEV1 under 50.
Can be considered if FEV1 over 50% and symptomatic with exercise limitation
Ideal candidates for LVRS
(a) Location of emphysema
(b) Perfusion to upper lobes
(c) Severity of air trapping (RV)
(d) Severity of obstruction (FEV1)
(e) Hypercapnia
Lung volume reduction surgery
(a) Apical predominant, ideally heterogeneous emphysema
(b) Reduced perfusion (under 10%) to upper lobes.
If perfusion is preserved (over 20% to upper lobes on V/Q scan) tells you pt is still using those upper lobes and LVRS may not improve V/Q so much
(c) Severe air trapping with RV over 150%
(d) Severe obstruction but not too severe, typically FEV1 between 20-45%
(e) No hypercapnia, pCO2 under 60
Aside from CT chest what eval is needed to assess candidacy for LVRS?
(a) ABG
(b) PFTs
(c) TTE
(d) V/Q
Of course get CT chest to show distribution of disease: ideal is upper lobe and heterogeneous
Then also get
-ABG to r/o significant hypercapnia (pCO2 over 60)
-PFTs to ensure significant air trapping (RV over 150%) and obstruction (FEV1 20-45%)
-TTE to r/o significant PH
-V/Q to assess perfusion to upper lobes
Indication for home non-invasive PPV in COPD pts
-Chronic hypercapnia (pCO2 over 52)
NIPPV also reduces readmission rates if pCO2 elevated on discharge for acute COPD exacerbations
AND
-nocturnal hypoxia
AND
-documentation that OSA has been ruled out
So- can quality for bipap if hypoxic and hypercapnic w/o OSA
Cataplexy
(a) What is is
(b) Associated with what diagnosis
Cataplexy = weakness during periods of strong emotions, pathognomonic symptom of narcolepsy
What are the variables of STOP-BANG
(a) Cutoff for likelihood of OSA
S-snoring loudly
T- tiredness
O- observed apnea
P- pressure (HTN)
B- BMI 35 or above
A- age 50 or above
N- neck circumference 16 or above for M
G- Gender (male)
(a) 3 or above indicative of high-likelihood of OSA
Epworth sleepiness scale- what score is consistent with pathologic sleepiness
Epworth sleepiness scale- likelihood of falling asleep 0 to 3 during 7 different activities
-sitting and reading, watching TV, passenger in a car etc
Score ranges from 0 to 24, score over 10 associated with pathologic sleepiness
Some features of narcolepsy
Narcolepsy- REM at abnormal times
-sleep paralysis
-cataplexy (weakness during periods of strong emotions))
-hyponogogic hallucinations = vivid visions while falling asleep or while awakening, thought to be a mix of wakefulness during REM
How to differentiate central from obstructive apneas on PSG
Obstructive- persistent respiratory effort without airflow
Central- complete absence of respiratory effort during cessation of airflow
AHI cutoffs for normal
mild
moderate
severe OSA
AHI cutoffs
Normal under 5 events/hour
Mild: 5-14 events/hour
Moderate: 15-29 events/hour
Severe: over 30 events/hr
Differentiate apneas and hypopneas
Apnea = at least 90% reduction in airflow for two or more breaths
Hypopneas = at least 30% reduction in airflow associated with either arousal or desat of at least 3%
Define AHI
Apnea hypopnea index = amount of apneic (at least 90% reduction in airflow) + hypopnic (at least 30% reduction in airflow with eitehr desat or arousal) per hour
Differentiate OHS from sleep-induced hypoventilation
OHS- BMI over 30 with PaCO2 over 45 while awake with other caused of hypercapnia ruled out
Most OHS is associated with OSA, small percent associated with Sleep-induced hypoventilation: PaCO2 over 55 for at least 10 minutes while sleeping
What on sleep study hints that you may need Bipap instead of CPAP for OHS related to OSA?
Crank up CPAP until obstruction is relieved but still see hypoxia => another cause of hypoxia such as hypoventilation
Swith to bi-level PAP with delta P of 8-10 to help ventilate
Differentiate BPAP and ASV (adaptive support ventilation)
BPAP- set an IPAP and EPE
-for OSA, hypoventilation, neuromuscular disease, pulmonary edema, COPD exacerbation
ASV- set EPAP, min/max PS, and a backup rate
-for hypoventilation, central sleep apnea, complex apnea (mixed obstructive and central)
Differentiate solitary pulmonary nodule vs. mass
Solitary pulmonary nodule: under 3cm with normal surrounding lung parenchyma
Over 3cm = mass
Differentiate concerning vs. benign calcification patterns of a solitary pulmonary nodule
65M smoker with COPD (FEV1 40%) with 1.5cm ground glass RUL lesion
Next mgmt step?
Ground glass lesion under 3cm, over 6mm = repeat CT chest in 6-12 months
Contrast Fleischner society guidelines for solid vs. subsolid single lung nodules
(a) Size cutoffs
Fleischner society guidelines for SPN
Solid nodules split by low and high risk patients
-single solid nodule under 6mm in low risk pt: no f/u, in high risk pt: option CT at 12 months
-single solid nodule 6-8mm in both low and high risk pts: CT 6-12 months
-single solid nodule over 8mm in both low and high risk: CT 3 months vs. PET vs. tissue sampling
Subsolid nodules just split by 6mm cutoff and by ground glass vs. subsolid
-GG and subsolid under 6mm: No f/u
-GG over 6mm: repeat CT in 6-12 months
vs. subsolid over 8mm: repeat CT 3-6 months
Contrast Fleischner society guidelines for ground glass v. part solid ‘subsolid’ single pulmonary nodules
Split by 6mm cutoff
Ground glass nodule under 6mm- no f/u
GG nodule over 6mm: CT at 6-12 months, then CT every 2 years until 5 years
Part solid nodule under 6mm- no f/u
Part solid nodule over 6mm: CT at 3-6 months (so earlier) then annually for 5 yrs
Fleischner society guidelines- who gets repeat CT for SPN under 6mm?
Optional f/u CT scan for high risk in solid lesion
Otherwise low risk solid nodule, GG or subsolid nodule all don’t require f/u if under 6mm
Flesichner society guidelines for multiple pulmonary nodules
Multiple pulmonary nodules
-under 6mm no f/u
-over 6mm for both solid and subsolid: f/u CT in 3-6 months
Lofgren syndrome
(a) Diagnostic relevance
Lofgren syndrome- characteristic of sarcoidosis
-Bilateral hilar lymphadenopathy
-Erythema nodosum
-Migratory polyarthralgias
(a) Doesn’t require biopsy b/c so highly probable for sarcoid
Common extrapulmonary manifestations of sarcoidosis
(a) Skin
(b) Ocular
Sarcoidosis
(a) Skin- lupus pernio (chronic raised indurated lesion over nose), erythema nodosum
(b) Ocular- uveitis, optic neuritic
Describe the panda sign on gallium scan
(a) Suggestive of what diagnosis?
Bilateral involvement of parotid and lacrimal glands
(a) not specific (can also be seen in Sjogrens or lymphoma) but
suggestive, and can be supported by mediastinal lymphadenopahty
Lofgren syndrome:
(a) Diagnostic steps required
(b) Management
Lofgrens; bilateral hilar lymphadenopathy, migratory polyarthralgias (ankle, knees), erythema nodosum, fever
(a) No biopsy required b/c such high likelihood of sarcoid
(b) Mgmt- typically self resolves or can use NSAIDs
Lab values to check annually for sarcoidosis maintenance (screening of extrapulmonary manifestations)
-Cr
-Ca
-1,25-OH vitamin D
-LFTs including alk phos alk phos: not uncommon to have cystic bony lesions
Average steroid dose for initial treatment of sarcoidosis?
Prednisone 20-40mg (typically don’t need the higher .5mg/kg situation)
When to add steroid-sparing agent for treatment of sarcoidosis
Start sarcoidosis treatment with steroids (typically prednisone 20-40mg daily) x3-6 months, then start to taper
If can taper steroids to under pred 10mg daily can just continue the pred, but if tapering below pred 10mg causes recurrence of symptoms => add steroid-sparing agent (typically MTX, occasionally plaquenil)
When to use MTX vs. plaquenil for sarcoidosis treatment?
MTX first line for sarcoid with cardiac involvement
Plaquenil (hydroxychloroquine) much weaker- can used as add on or for troublesome skin involvement or hypercalemia
For pulmonary sarcoidosis (not extrapulmonary)- when to consider treatment
Minimal symptoms (Ex: cough alone)- consider ICS
Moderate disease with CXR stage II (nodal enlargement + parenchymal involvement), abnormal PFTs, dyspnea- oral steroids- typically prednisone 20-40mg daily x3-6 months
Major drugs that cause drug-induced sarcoidosis-like reaction
Drug-induced sarcoid-like reactions (drug hypersensitivity with granuloma formation)-
immune checkpoint inhibitiors
interferons
TNFalpha antagonists: infliximab
BAL neutrophilia (over 50%) seen in what aside from pulmonary infections?
BAL neutrophilia in infection, AIP, DAD, acute exacerbation in IPF
Which IPFs to expect BAL lymphocytosis (over 25%)
Cellular NSIP, sarcoid, HP, LIP
2 AIDS-defining malignancies
- Kaposi sarcom
- Non-Hodgkin Lymphoma
Typical CT chest findings of pulmonary Kaposi’s sarcoma
Up to 30% of Kaposi’s can exist in the lungs without mucocutaneous involvement
- peribronchial/perilymphatic ‘flame’-shaped densities
- pleural effuions
- lymphadenopathy
- airway lesions
At what CD4 count start to worry about the following
(a) PJP
(b) LIP
(c) Aspergillus
CD4 count
(a) PJP under 200
(b) LIP under 500- not strong association with lower CD4 count, suggesting need some degree of immune system activity present
(c) Aspergillus PNA under 50
At what CD4 count start to worry about the following
(a) CMV PNA
(b) Histo/coccidio/toxo
(c) Disseminated TB
CD4 count
(a) CMV PNA under 50
(b) Disseminated histo and coccidio under 50, while toxo pneumonitis under 100
(c) Disseminated Tb under 200
At what CD4 count to start to worry about:
(a) Pulmonary kaposi sarcoma
(b) Pulmonary crypto
(c) Disseminated coccidio
CD4 count
(a) Pulmonary Kaposi under 100
(b) Cryptococcal PNA under 200
(c) Disseminated coccidio and histo under 50
