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CM Pulmonary Boards > Infection, COPD, Asthma > Flashcards

Infection, COPD, Asthma Flashcards

1
Q

Differentiate acute bronchitis and bronchiolitis

A

Bronchitis = inflammation of larger and midsize airways, typically viral, normal CXR self-limited x3 weeks

Bronchiolitis- inflammation of bronchioles (smaller airways) again mostly viral (RSV)

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2
Q

Main use/indication for flucytosine

A

Replication inhibitor, use as adjunct for candida and cryptococcus

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3
Q

Differentiate mechanism of antifungals

(a) amphotericin B
(b) azole
(c) echinocandins

A

Antifungal mechanism

(a) Amphotericin = disturbs cell membrane by binding to ergosterol (main sterol in fungal membrane)
(b) Azoles- inhibits ergosterol synthesis => cell membrane dysfunction
(c) Echinocandins (micafungin, caspofungin)- 1,3-beta D glucan synthetase in cell wall

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4
Q

Main indications for echinocandins (caspo/mica)

A

Echinocandins- only IV
Indications: empiric tx of neutropenic fever, candidemia, invasive aspergillus

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5
Q

First line treatment for mucormycosis

A

Invasive mucor tx: surgical debridement for source control with amphotericin B

Step-down once responding to posaconazole or isavuconazole
-posaconazole second line/salvageif ampho not tolerated

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6
Q

What can cause a false positive galactamannan

A

Antibiotics, mainly zosyn and augmentin

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7
Q

Describe spectrum of disease caused by aspergillus and risk factors

A

Depends on degree of immunosuppression, worsening immune status

(Least immunosupp)
Allergic: ABPA
Chronic/cavitary: aspergilloma, chronic cavitary aspergillosis
Semi-invasive: chronic necrotizing aspergillosis
Invasive: invasive pulmonary aspergillosis, tracheobronchial aspergillosis
(Worsening immune status)

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8
Q

Which antifungals have activity against aspergillus?

A

Active against aspergillus: voriconazole, itraconazole, amphotericin B

NOT fluc!

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9
Q

Limitation of micafungin for candidemia

A

Echinocandins lack good eye penetration => if candida endopthalmitis seen on dilated retinal exam need to add fluconazole or amphotericin B

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10
Q

Antifungals to avoid in pregnancy

A

First line- amphotericin, echinocandins, azoles except vori are category C

Contraindicated: flucytosine and voriconazole given fetal abnormalities in animal studies

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11
Q

Some clinical differentiating factors from pulmonary mucormycosis and invasive pulmonary aspergillus

A

Clinically both can have diffuse pulmonary nodules in immunocompromised patient

-more nodules (over 10) or presence of pleural effusions favor mucor (pleural effusions uncommon in invasive pulmonary aspergillosis)
-sinopulmonary or angioinvasive involvement favor mucor

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12
Q

Mucormycosis

(a) Particular risk factor
(b) Typical extrapulmonary manifestations

A

Mucor

(a) Immunocompromised, poorly-controlled diabetics
(b) Sinupulmonary (ENT), angioinvasive (vessels)

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13
Q

Cryptococcus neoformans

(a) Particular risk factor
(b) Utility of serum cyptococcus antigen in pulmonary disease

A

Cryptococcus neoformans

(a) HIV, post-transplant
(b) Serum crypto not very sensitive for limited pulmonary disease, very sensitive in disseminated disease

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14
Q

Tx of cryptococcus neoformans

(a) Mild pulmonary disease
(b) Severe pulmonary disease or CNS Involvement

A

Cryptococcus neoformans treatment

(a) Mild pulmonary disease alone (w/o CNS involvement) = fluconazole 6-12 months
(b) Severe pulmonary disease or CNS involvement = induction with amphotericin and flucytosine
then consolidation and maintenance with fluconazole (higher dose x8 weeks then lower dose for at least a year)

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15
Q

Which endemic mycosis most clearly mimics sarcoidosis (and must be ruled out prior to starting immunosuppression)

(a) How to rule out

A

Histoplasmosis (Mid W and S central US, Ohio and Mississippi River Valley)- calcifications, granulomas, extensive nodularities, and mediastinal lymphadenopathy (mimics sarcoid closely)

(a) Serum and urine histo Ag together have over 90% sensitivity
(b) If very concerned can do histology: caseating granulomas and narrow-based budding yeast

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16
Q

Cryptococcus vs. coccidio

(a) Risk factor
(b) Most common manifestation

A

(a) Cypto- more immunocompromised, HIV
Most common disseminate into CNS, also with limited pulmonary and disseminated pulmonary disease

(b) Coccidio- more endemic to SW (Arizona)
local, diffuse, and fibrocavitary PNA

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17
Q

What extrathoracic findings suggest histoplasmosis as the cause of a patient’s fibrosing mediastinitis?

A

Fibrosing mediastinitis (PH risk factor) look for splenic and liver calcifications to suggest histo

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18
Q

Fungal infection with classic presentation of rose gardener injuring finger with a thorn

(a) Tx

A

Sporothrix schenckii- fungus typically cutaneously inoculated
-typically causes lymphocutaneous features, can cause chronic cavitary fibronodular disease

(a) Itraconazole

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19
Q

General tx differentators for endemic mycoses

A

Histo, coccidio, blasto, and paracoccidio all treated similarly

If mild disease/only pulmonary- itraconazole

If severe disease (hypoxia, diffuse imaging findings, extrapulmonary manifestations)- amphotericin then itraconazole

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20
Q

Noninvasive testing for endemic mycoses

(a) Histo
(b) Coccidio

A

Noninvasive testing for endemic mycoses

(a) Histo- urine and serum histo Ag, when together are 90% sensitive for disease
(b) Coccidio- Cocci IgG and IgM antibodies for screening,

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21
Q

Which endemic mycosis is associated with PH specifically due to fibrosing mediastinitis?

A

Histoplasmosis (Ohio/Mississippi river valley) can cause fibrosing mediastinitis, risk factor for PH

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22
Q

How to differentiate sarcoidosis and histoplasmosis on histology

A

Both sarcoid and histo can look very similar on imaging: diffuse nodules, mediastinal lymphadenopathy, calcifications

Histology- both granulomas
Sarcoid- noncaseating granulomas diffuse
Histo- caseating granulomas with fungal elements (narrow based budding yeasts)

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23
Q

Indications for steroids in PJP treatment

A

Steroids indicated for:

-PaO2 under 70mmHg, SpO2 under 92% on room air (aka any hypoxia)
-Aa gradient over 35

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24
Q

Name the most common of the following diseases associated with HIV

(a) Malignancy
(b) Interstitial pneumonitis
(c) Vascular complication

A

HIV-associated

(a) Malignancies- Kaposis sarcoma (most common), then non-Hodgkin’s lymphoma
(b) Lymphoid interstitial pneumonitis (LIP)- cystic lung 54321disease
(c) Vascular complication- group I PAH

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25
Q

CD4 cutoffs for infectious prophylaxis in AIDS patients

A

CD4 under 200: PJP ppx with bactrim (typically 1 DS TIW)

CD4 under 100: already on bactrim, but also now covering for toxo ppx

CD4 under 50: consider azithro for MAC ppx but not always necessary if starting ART (data for azithro ppx is pre-ART)

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26
Q

Which HIV patients get screened with quantiferon?

A

All of them! All HIV patients should be screened for LTBI with quant

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27
Q

At what CD4 count do you expect the following

(a) PJP
(b) CMV
(c) Kaposi sarcoma
(d) Toxo

A

(a) PJP at CD under 200
(b) CMV under 50
(c) Kaposis under 100
(d) Toxo under 100

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28
Q

Name two filamentous bacteria that cause pulmonary cavitation

A

Typical filamentous bacteria causing pulmonary cavitation = actinomyces and nocardia

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29
Q

Actinomyces vs. nocardia

(a) Imaging features
(b) Treatment

A

(a) Imaging:
Consider both for nonresolving PNA, especially if cavitary
if involves pleura or chest wall think actino

(b) Tx:
Actino- PCN
Nocardia- TMP-SMX

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30
Q

Actinomyces vs. nocardiac

(a) Which expected in immunocompetent patient
(b) Which sulfur granules
(c) Which weakly AFB positive
(d) Which associated with cervicofacial abnormalities

A

(a) Immunocomptent- expect actino
(b) Sulfur granules = grouped actino filaments
(c) Weakly AFB positive gram positive aerobe = nocardia
vs. not AFB positive gram positive anerobe = actino
(d) Actino associated with cervicofacial abnormalities

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31
Q

Candidemia treatment

(a) Preferred initial agent

Duration of tx
(b) With endopthalmitis
(c) W/o endopthalmitis

A

Candidemia

(a) Start with echinocandin (micafungin) at least until know sensitivities

Duration of tx:
(b) With endopthalmitis: 4-6 weeks
(c) Without: 2 weeks from negative cultures

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32
Q

Regular surgical facemask vs. N95

(a) VZV PNA
(b) Influenza

A

(a) VZV extremely infectious- wear N95
(b) Influenza- large droplets, regular surgical facemask adequate

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33
Q

Differentiate yeast and mold

(a) Explain how a fungi can be dimorphic

A

Fungi can exist in two forms: unicellular yeast or multicellular mold (multicellular hyphae)

(a) Dimorphic fungi [ex: endemic mycoses] are yeast at cold temp, mold at hot/body temp
-fungi can be different forms depending on temperature, pH, cysteine levels

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34
Q

Differentiate which patient/risk factors get

(a) ABPA
(b) Aspergilloma
(c) Chronic necrotizing aspergillosis
(d) Invasive pulmonary aspergillosis

A

Ubiquitous exposure to aspergillus, then underlying immune status dictates what disease pt develops

(a) Overactive, atopic immune system- think ABPA
(b) Pre-existing cavity- aspergilloma (won’t just form a fungal ball on its own)
(c) Mild immunosuppression with potentially COPD- chronic necrotizing aspergillosis
(d) Neutropenic => IPA

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35
Q

Classic imaging feature of aspergilloma ‘fungal ball’

A

Moves within the cavity in supine vs. upright films

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36
Q

Differentiate clinical manifestations of chronic necrotizing aspergillus from invasive pulmonary aspergillosis

A

Clinical presentation

-chronic necrotizing aspergillus in mildly immunosuppressed pt: insidious onset, think of in PNA that just won’t go away
vs.
-IPA: nodules, cavitary lesions, acute systemic infectious signs

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37
Q

ABPA diagnostic criteria

(a) Predisposing conditions
(b) Mandatory major
(c) 2 of 3 minor ABPA

A

Diagnostic criteria for ABPA:

(a) Have to either be asthmatic or CF pt
(b) With elevated IgE (typically over 1000) and positive aspergillus skin test or elevated anti-A fumigatus IgE

(c) 2 of 3 minor criteria
-A fumigatus IgG
-radiogrpahic pulmonary opacities (mucus plugging)
-total eos over 500

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38
Q

Typical management of ABPA

A

Steroids +/- itraconazole

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39
Q

Middle-aged M returns from hunting trip in Arkansas with respiratory illness and infiltrates not responsive to abx. Dog also acutely ill

A

Arizona- just W of Mississippi, N of Texas, right in that Mississippi River Valley which puts at risk for both histo and blast

-dogs also get infected with blasto

Blasto! broad-based budding yeasts with bubba (bubba the dog)

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40
Q

Tx of blastomycosis in pregnancy

A

Need to avoid azoles in pregnancy so for all endemic fungi (histo, coccidio, blasto, paracoccidio) use amphotericin

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41
Q

What fungi does beta-D glucan NOT detect

A

Beta-D glucan good for invasive aspergillus, invasive candidiasis, and other invasive mycoses EXCEPT does NOT detect mucor and crypto

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42
Q

Endemic mycoses classic for

(a) Skin involvement
(b) Valley fever
(c) Bird/bat droppings
(d) Spelunking, chicken coops

A

Endemic mycoses

(a) Skin involvement- violaceous ulcerating lesions in blastomycosis
(b) Valley fever = coccidiodomycosis, SW US
(c) Bird/bat droppings as reservoir for histo
(d) Spelunking and chicken coops as place of transmission for histo

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43
Q

Describe these unique manifestations of histoplasmosis

(a) Bronchiolithiasis
(b) Fibrosing mediastinitis

A

Histplasmosis- calcifying, necrotizing granulomas

(a) Bronchiolithiasis- calcified eroding nodes
(b) Fibrosing mediastinitis- mediastinum hardens like cement, can cause mass effect on vessels (PH) and airways

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44
Q

Describe link between defuroxime and certain fungal infection

(a) Which infection
(b) Mechanism

A

Defuroxime (iron chelators) put pts at increased risk for
(a) Mucormycosis
(b) Something to do with iron overload, possible that patients in DKA have more iron available which is a substrate for mucor growth

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45
Q

Standard duration of bactrim for PJP treatment

A

PJP: bactrim x21 days

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46
Q

Antimicrobial regimen options for PJP treatment in pts with sulfa allergy

A

If can use TMP-SMX

Mild disease
-TMP (trimethoprim) and dapsone
-atovaquone

Severe disease
-clindamycin and primaquine
-IV pentamidine

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47
Q

Differentiate galactomannan and beta-D glucan

A

Both serum assays developed to detect invasive aspergillosis, beta-D glucan more sensitive but less specific

-galactomannan more specific for asperillus
-beta-D glucan also for invasive candidiasis and other invasive mycoses EXCEPT for mucor and crypto

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48
Q

Compare % risk of Tb reactivation in general population vs. HIV pt

A

General population: 5-10% lifetime reactivation risk, 50% of which is within the first 1-2 years after exposure

While HIV patients have about 5% risk of conversion annually

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49
Q

Define MDR TB

A

MDR Tb = resistant to both INH and rifampin

-considered a precursor to XDR-Tb

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50
Q

Define XDR-TB

A

XDR-Tb = MDR Tb (resistant to INH and rifampin) AND fluoroquinolone (moxi or levaquin) AND to one of the second line IV agents (amikacin, kanamcin, capreomycin)

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51
Q

Sensitivity of

(a) AFB smear in cases of active Tb
(b) Gene Xpert in smear positive Tb
(c) Gene Xpert in smear negative Tb

A

Sensitivity of test

(a) AFB smear in active Tb about 70% (so about 30% of active Tb cases will be smear negative, hence why culture is gold standard)

(b) Gene XPert (PCR) about 99-100% sensitive in smear positive Tb

(c) Gene Xpert about 85% sensitive in smear negative

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52
Q

How does gene Xpert detect rifampin resistance?

A

PCR for rpoB gene which accounts for over 90% of rifampin resistance

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53
Q

Can smear negative still transmit Tb?

A

Yes- smear negative can still be contagious

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54
Q

If bronching a patient to r/o Tb what else is a good idea?

A

Do post-bronch AFB culture! high yield and sometimes the only thing that is positive

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55
Q

After what duration of tx can active Tb pt be considered noninfectious?

A

After 2 weeks of treatment can be considered noninfectious

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56
Q

Differentiate radiographic findings of Tb reactivation from primary disease

A

Classic radiogrpahic findings of

(a) Tb reactivation: upper and posterior lobe predominant cavitation

(b) Primary disease- necrotic/calcified lymphadenopathy, pleural effusion, miliary disease

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57
Q

4 instances where Tb treatment requires extension from 6 to 9 months

A

-CNS tb
-severe cavitary disease
-if PZA cannot (or is not) used for the first two months
-if sputum does not convert by 2 months (obv also check sensis then too)

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58
Q

IRPE alteration typically required to treat HIV pts with Tb

A

Rifampin typically interferes with ART => use rifabutin for fewer drug drug interactions

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59
Q

How to change LTBI tx for HIV patients

A

RIfabutin often used in place of rifampin due to drug drug interactions with ART

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60
Q

Drugs to consider in treatment of MDR-Tb

A

US: first line for MDR-Tb 18 months of bedaqueline, linezolid, floroquinolone, clofazimine

or BPaL = bedaqueline, pretomanid, lienzolid

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61
Q

When to start ART in relation to IRPE for Tb treatment HIV patients

A

If CD4 count under 50 improves mortality to start ART within 2 weeks of Tb treatment

-otherwise not huge rush but start within 1-2 months

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62
Q

Which environmental exposure is specifically correlated to higher risk of Tb reactivation

A

Silicosis- thought to be mediated by detrimental effect of silica on alveolar macrophages

exposure- mining, sandblasting, construction

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63
Q

Benefit of BCG vaccine

A

Has been shown to prevent meningeal (CNS) and miliary Tb in children

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64
Q

Differentiate classic imaging findings of primary Tb vs. reactivation

A

Imaging findings

Primary Tb: middle and lower lobe predominance with ipsilateral hilar lymphadenopathy

Reactivation: upper lobe predominance with cavitation

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65
Q

CSF studies characteristic of Tb meningitis

A

Tb meningitis

-elevated white count (100-500) with lymphocytic predominance
-elevated opening pressure
-elevated CSF protein (100-500, normal under 40)
-low CSF glucose (under 10)

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66
Q

2 ways in which CNS involvement of Tb alters treatment

A

CNS Tb

-extends treatment from 6 to 9 months
-add steroids

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67
Q

Which bacterial cause of CAP associated with

(a) Most common etiology of post-influenza PNA
(b) Severe necrotizing disease
(c) Gram negative in those w/ underlying lung disease (COPD, CF), hint not pseudomonas
(d) Severe infection in asplenic pts

A

Bacterial CAP

(a) Post-influenza PNA: strep pneumo (also most common overall)
(b) Necrotizing/cavitary or empyema raises suspicion for staph aureus
(c) H. influenza
(d) Strep pneumo (encapsulated)

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68
Q

Which bacterial cause of CAP associated with

(a) Hemolytic anemia
(b) Exposure to contaminated water

A

CAP causes

(a) Hemolytic anemia associated with mycoplasma- cold agglutinin due to IgM autoantibodies
(b) Legionella- contaminated water, cruise ships

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69
Q

Causative organism for PNA associated with exposure to

(a) Wild rodents
(b) Bat droppings
(c) Birds
(d) Rabbits
(e) Farm animals

A

Exposures causing PNA

(a) Wild rodents, especially in SW US = hantavirus
(b) Bat droppings = histoplasmosis
(c) Birds = chlamydia psittaci (psittacosis)
(d) Rabbits = francisella tularensis
(e) Farm animals = coxiella burnetti (Q-fever)

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70
Q

Current PNA vaccine guidelines

(a) What vaccine
(b) For what groups

A

PNA vaccine

(b)-all pts over 65 OR
under 65 with another comorbidity: COPD, CHF, DM, DM, EtOH, asplenic

(a) Either PCV-20 alone or
PCV-15 then one year later PPSV-23

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71
Q

What does ceftaroline cover?

A

Covers MRSA
does NOT cover pseudomonas

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72
Q

Allergy to what cephalosporin makes you cautious before using aztreonam

A

Aztreonam can be used safely in those w/ cephalosporin allergy except prior serious reaction to ceftazidime given similar side chain => higher risk of cross reaction

(sidebar ceftazidime = 3rd gen cephalosporin like ceftriaxone and cefpo)

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73
Q

MAC ppx in HIV patients

(a) When indicated
(b) What med

A

MAC ppx in HIV pts with CD4 under 50 with azithro (or clarithro)

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74
Q

Differentiate treatment for M. kansasii and M. abscessus

A

Slow-growing NTM = MAC and M. Kansasii- both same tx of azithro, rifampin, ethambutol

Rapid-growing M. abscessus- much more complicated tx based off sensitivities: clofazimine, amikacin, cefoxitin, imipenem, linezolid

75
Q

80F with productive cough x4 years and RML bronchiectasis, two recent sputum samples one with MAC one with M. kansassi

Next step

A

Stupid trick question-

Either get another sputum or undergo bronch for additional cultures b/c one sputum culture doesn’t prove disease

Once have two + imaging features + clinical features can treat: for both slow-growing NTMs (MAC and M. kansassi) tx is the same with azithro, rifampin, ethambutol x12 months from sputum conversion

76
Q

Risk of reactivation of LTBI for pt on TNFalpha blockers compared to not

A

Pts on anti-TNF have 12x increased risk of LTBI activation

77
Q

Differentiate activity of the following in asthma

(a) IL-4
(b) IL-5
(c) IL-13

A

Role of the following cytokines, all released by Th2 cells

(a) IL-4: secreted by basophils to stimulate B-cells to make IgE
(b) IL-5 regulates eosinophil production and maturation
(c) IL-13 secreted by basophils and Th2 cells
-stimulates B-cells to make IgE (like IL-4)
-stimulates degranulation of mast cells to release proinflammatory mediators

78
Q

Pathophysiology of changes in asthma by layers of the bronchial epithelium

(a) Goblet cells
(b) Basement membrane
(c) Subepithelium
(d) Smooth muscle

A

Epithelium

(a) Goblet cell hyperplasia => more mucus to plug airways
(b) Basement membrane thickening
(c) Subepithelial fibrosis
(d) Smooth muscle hyperplasia => worsening bronchospasm

79
Q

Differentiate role of Th1 and Th2 in asthma

A

Th1 to recruit neutrophils

Th2 to stimulate IgE synthesis, stimulate mast cell production and degranulation, stimulate eosinophil production and migration

80
Q

Which PFT loops expected in larygneal dysfunction?

A

Flattening during inspiratory loop (C) consistent with extrathoracic obstruction

81
Q

Describe the PC20 used during methacholine bronchoprovocation test

A

PC20 = concentration of drug (typically methacholine) that causes a 20% drop in FEV1, this is when the provocation test is stopped

PC20 at or under 8 has good negative predictive value for asthma

82
Q

Differentiate occupational asthma and reactive airway dysfunction syndrome

(a) Which will be reproducible by inhalation challenge
(b) Duration of symptoms

A

Occupational asthma- immunologic phenomenon (sensitization to allergen, IgE involved) only have symptoms at work
(a) Reproduced by inhalation challenge of small amounts of allergen b/c immunologic pathway
(b) Symptoms improve after work or during holidays/weekends

vs.
RADS- abrupt onset of symptoms following exposure
(a) Not reproduced by inhalation challenge b/c not immunologic, due to intensity and duration of exposure
(b) Symptoms can persist after exposure

83
Q

Triad of aspirin sensitivity and asthma

(a) Presumed mechanism- IgE?
(b) Tx

A

Samter’s triad = asthma, chronic rhinosinusitis w/ nasal polyps, ASA (COX-1 including ASA and NSAID) sensitivity

(a) Not IgE! thought to be a ‘pseudoallergy’ of an abnormal response to NSAID exposure due to inability to breakdown byproduct
(b) Tx- typical asthma tx, intranasal glucocorticoids, leukotriene inhibitor ** (montelukast)

84
Q

When to consider ASA desensitization in pt with aspirin-exacerbated respiratory disease

A

-refractory nasal polyposis (to intranasal steroids and even surgery)
-strong indication for ASA (ex: PCI)
-strong indication for NSAID (ex: inflammatory condition)

85
Q

What symptoms trigger change in treatment from PRN ICS-formoterol to maintenance?

A

PRN to maintenance when symptoms go from intermittent (less than 2x/week, no nightnighttime awakenings, no limitation w/ normal activity) to mild persistent (symptoms or SABA use more than 2x per week, 3-4 per month nighttime awakening, minor interference with normal activity)

86
Q

Differentiate intermittent and persistent asthma

(a) Tx

A

Intermittent asthma- symptoms or SABA use less than 2x week, less than 2x/month nighttime awakenings, no limitation of normal activity
(a) Tx- PRN low-dose ICS-formoterol, can consider standing low-dose ICS

Persistent- mild when symptoms more than 2 days a week but not daily (moderate)
Nighttime awakening 3-4 times a month but not yet weekly (moderate)
Mild interference w/ normal activity
(a) Tx- standing low-dose ICS, LABA

87
Q

Differentiate mild, moderate, severe persistent asthma

(a) Inhaled treatment stepup

A

Persistent once symptoms more than 2x/week, nighttime awakenings more than 2x/month

Mild: symptoms (or SABA use) more than 2x a week, nighttime awakenings 4 or more per month (but not weekly), mild interference with normal activity
(a) Maintenance low dose ICS-LABA

Moderate: symptoms (or SABA use) daily, nighttime awakenings at least once a week (but not nightly), moderate interference w/ normal activity
(b) Maintenance medium/high dose ICS-LABA

Severe: symptoms (or SABA use) throughout the day, nighttime awakenings almostly nighly
(b) Maintenance high dose ICS-LABA, add LAMA, adjunctive tx (Mabs, bronchial thermoplasty) etc

88
Q

50M s/p renal transplant on MMF, tacro, pred p/w cough, fever, draining skin lesions
CXR attached, gram stain attached

(a) most likely dx
(b) next mgmt step

A

PNA in immunocompromised, gram stain with gram positive (purple) branching/filamentous bacteria = nocardia

(a) Nocardia
(b) CNS imaging given propensity of nocardia to have extrapulmonary symptoms (skin and CNS)

89
Q

Differentiate appearance of gram positive vs. gram negative on gram stain

A

Gram stain: purple stain that then the thick cells walls of gram positive organisms keep it purple

Thin cell walls of gram negative => don’t hold on to purple so are pink

90
Q

Bioterrorism agents:
francisella tularensis vs. yersinia pestis

(a) Vector
(b) Tx

A

Francisella tularensis

(a) Rabbits
(b) Aminoglycosides (gentamycin, streptomycin)

Yersinia pestis = plague!
(a) Rodents
(b) Gentamycin

91
Q

Differentiate gram-negative rods by lactose vs. non-lactose fermenters

A

Gram negative rods

Non-lactose fermenters: pseudomonas, proteus
Lactose-fermenting: serratia, E. coli, klebsiella, enterobacter

92
Q

Pertussis

(a) Typical clinical presentation
(b) Tx

A

(a) Prodromal phase which fever, rhinorrhea, sore throat (mimics viral URI) then persistent whopping cough w/ possible spasms, possibly associated with emesis
Typically self resolves

(b) Azithro for ppl with suspected (or proven) pertusis with symptoms for 4 weeks or less
-after 4 weeks azithro not shown to do anything

93
Q

36M s/p renal transplant p/w SOB, fever, night sweats after failing levaquin.

BAL AFB, gram stain, CXR below

(a) Dx
(b) Tx and duration

A

AFB+, positive gram stain with purple = gram positive organism

Gram positive organism causing pulmonary consolidation in immunocompromised = nocardia (a)

(b) Bactrim + amikacin, keep amikacin until sensitivities known
Duration: 6-12 months, if continued immunosuppression use lifelong secondary prophylaxis

94
Q

New HIV+ (CD4 30) Tb diagnosis

Treatment

A

IRPE
-ART within 2 weeks (better outcomes for CD4 under 50 if started within 2 weeks, otherwise can wait for up to 12 weeks)

PLUS steroids (prednisone) within 4 weeks given 50% change of Tb-IRIS for HIV pts with CD4 under 100

95
Q

Which carbapenem does NOT cover pseudomonas?

A

Ertapenem- nice b/c daily administration but does not cover pseudomonas

While meropenem and imipenem covers pseud

96
Q

Pseudomonas resistant to cefepime, mero, avycaz

Next-line agent?

A

Cefiderocol = siderophore cephalosporin (inhibits bacterial cell wall synthesis)
-good for extremely resistant gram negatives such as pseudomonas, acinetobacter, E. coli, klebs, and serratia

Colistin next in line but choose cefiderocol first b/c colistin has high toxicity/side effect profile

97
Q

23F no PMH works in pet store: grooms exotic birds, cleans bird cages p/w days of fevers, headaches, cough. Mild splenomegaly and patchy basilar predominant infiltrates w/o lymphadenopathy

(a) Most likely dx
(b) Tx

A

(a) Psittacosis (parrot disease, parrot fever) from chlamydophila psittaci
(b) Tx- doxy

Bird droppings trigger thoughts of histo but endemic, not likely in immunocompetent, and would expect lymphadenopathy

98
Q

LTBI tx in HIV negative patient on OCPs

A

Have to avoid rifamycin agents b/c of interaction with OCPs => INH x6 months

99
Q

Top 3 immunosuppressing conditions that are associated with cryptococcus

A
  1. HIV
  2. Iatrogenic immunosuppression
  3. Cirrhosis
100
Q

Differentiate fungi based on the following histology

A

(a) PJP- round, oval, helmet shaped yeasts
(b) Thick-walled spherules = coccidio
(d) Narrow-based budding yeast in clusters inside macrophages = histo

101
Q

Two most common extrapulmonary sites of blasto

A

(1) Lungs
(2) Skin- verrucous lesion w/ irregular borders, can ulcerate and form microabscesses
(3) Bone and joint, osteomyelitis

102
Q

32F at 30 weeks gestation has influenza- mgmt?

A

Oseltamivir

-both oseltamavir and zanamivir are safe and effective in pregnancy, oseltamivir has better data in pregnancy so preferred

103
Q

33F with hacking cough x4 weeks after flu-like illness 6 weeks ago
-forceful coughs during expiration, sometimes w/ vomiting
-had all childhood vaccinations
-normal CXR

(a) Dx
(b) Mgmt

A

(a) Long pertussis, past the initial catarrhal phase (viral-like of rhinorrhea, malaise). then paroxysmal coughing phase which can persist 3-6 months

(b) After 4 weeks abx not recommended (before 4 weeks- use azithro) b/c it’s the toxins, not the bacteria itself that cause the cough => antibiotics do not offer clinical benefit in the paroxysmal phase

104
Q

Describe brief pathophysiology of abnormal balance of proteins in emphysema that causes destruction

A

Emphysema- inflammatory cells (neutrophils, macrophages) release tons of MMP (matrix metalloproteinases), proteases, and elastases causing destruction of elastin

105
Q

Presumed mechanism of cough in chronic bronchitis

A

Goblet cell hyperplasia => mucus impaction causing airway narrowing

Epithelial thickening and smooth muscle hypertrophy => airflow obstruction

106
Q

Annual expected drop in FEV1 after age 30 in

(a) Smokers
(b) Nonsmokers

A

(a) 60 ml annually
(b) Nonsmokers- 30ml annually

107
Q

Mechanism of emphysema in alpha-1 anti trypsin

A

Lack of alpha-1 anti trypsin protein which is the main anti-elastase enzyme to protect lung from elastin degradation

108
Q

High vs. low risk genotypes in alpha-1 anti trypsin deficiency

A

Low risk genotypes = MM, SS

High risk genotypes = ZZ, null

109
Q

Ratio of inspiratory capacity to what is an independent mortality predictor in COPD?

A

Inspiratory capacity to TLC (total lung capacity) under 25% is an independent predictor of mortality in COPD

110
Q

Differentiate GOLD A, B, C, D

A

GOLD 2x2
Y-axis:
FEV1: above or below 50%
Exacerbation history: high if one requiring hospitalization or 2 total in past 2 months
(go with the higher one)

X-axis = symptoms
Low: CAT under 10, mMRC 0-1
High: CAT above 10, mMRC 2 or above
(go with higher one)

111
Q

Utility of BODE index?

(a) Components

A

BODE index = 10 point scale to predict 4-year mortality in COPD. out-performs any single parameter

(a) BODE
B- BMI, lower BMI portends worse prognosis
O- obstruction based on %predicted FEV1
D- dyspnea based on mMRC
E- exercise based on 6MWT

112
Q

Asthma vs. COPD

(a) Type of lymphocytes implicated
(b) Cytokines mainly involved

A

Asthma
(a) Th2 (type 2 helper T cells), CD4+
Lymphocytes and eosinophils
(b) IL4, IL-5, IL-13

COPD
(a) Th1 (type 1 helper T cells), CD8+
Lymphocytes and neutrophils
(b) TGFbeta and TNFalpha, CXC (CXC chemokine), IL-8

113
Q

56F with COPD- dyspnea when hurrying on level ground. Post-BD FEV1 45% with no history of exacerbations

What GOLD combined assessment?

A

C

First column for symptoms (mMRC 1), higher column for FEV1 cutoff (under 50%)

????

114
Q

One way to differentiate COPD and asthma on spirometry

A

Asthma- technically reversible airway obstruction so expect ratio to improve (be above .7) post-bronchodilator

Of course can have more permanent airway remodeling with long-standing disease but generally COPD ratio stays under .7 while asthma improves w/ BD

115
Q

Compare smoking cessation aids: bupropion vs. varenicline

(a) Benefit
(b) Contraindications

A

Buproprion (wellbutrin) (a) doubles likelihood of quitting and improves abstinence at 1 year
(b) seizure d/o b/c lowers seizure threshold

Varenicline/chantix
(a) triples quit rate, increases abstinence at 6 and 12 weeks
(b) SI

(c) Head to head RCT varenicline (chantix) superior to buproprion

116
Q

Mechanism of roflimulast

(a) Indication

A

Roflumilast- PDE4 inhibitor

(a) Reduces exacerbation in chronic bronchitis phenotype (chronic cough) with FEV1 under 50% and history of exacerbations (2 or more in the yera)

117
Q

What non-pharmacologic intervention for COPD improves survival?

A

Supplemental O2 for those who meet criteria at rest (PaO2 under 55)

118
Q

Differentiate mechanism of ipratropium and tiotropium

A

Both muscaranic antagonists

(a) Ipratropium- SAMA, blocks M3 and M4 receptors
(b) Tiotropium- LABA, blocks M3

119
Q

Inhaled COPD med(s) that improve survival

A

None! All are to improve symptoms, reduce exacerbations and hospitalizations

None with proven survival benefit aside from LTOT (long term oxygen therapy)

120
Q

TORCH trial main takeaway for salmeterol/fluticasone (NEJM 2007)

A

TORCH trial- combo salmeterol/fluticasone (ICS/LABA) reduced exacerbations and hospitalizations vs. either alone

-no difference in mortality

121
Q

UPLIFT trial main takeaway for tiotropium (NEJM 2008)

A

UPLIFT- tiotropium (LAMA) reduced COPD exacerbations

-didn’t reduce rate of FEV1 decline or improve mortality

122
Q

Differentiate GOLD B and C

A

Numbers based on FEV1 cutoffs, letters based on symptoms and risk of exacerbation

B- high symptoms (mMRC 2 or above, CAT over 10) but low exacerbations (less than one in the past 12 mo, no hospitalizations)

C- low symptoms (mMRC 0-1 and CAT under 10), higher exac (2 or more in past 12 months or one hospitalization

123
Q

TORCH trial- adverse effect of ICS/LABA

A

Anything with ICS involved has increased risk of PNA

TORCH showing ICS/LABA reduced exacerbations/hospitalizations vs. either alone

124
Q

MCID for CAT score

A

2 points = minimal clinically important difference

125
Q

CD4/CD8 T-cells in

(a) Asthma
(b) COPD

A

(a) Most of asthma very active Th2 (CD4) cells, ‘type 2’ asthma

(b) While COPD more involved shift towards CD8 (Th1) cytotoxic T-cells

126
Q

Differentiate mMRC grade 1 and 2

A

0- breathless only with strenuous exercise

1- SOB when hurrying on level or walking up slight hill

2- walk slower than ppl of same age b/c of dyspnea, or have to stop when walking at own pace on level ground

3- stop for breath every 100m on level surface

127
Q

Tiotropium alone vs. salmterol alone to reduce COPD exacerbatons

A
128
Q

COPD mMRC dyspnea grade >2 symptoms, compare indacaterol/glycopyrronium vs. salmeterol/fluticaseone

A

LABA/LAMA reduced rates of annual COPD exacerbations vs. LABA/ICS

FLAME trial, NEJM 2016

129
Q

ETHOS trial for COPD, NEJM 2020

(a) Adverse effect of ICS

A

ETHOS trial, NEJM 2020- triple therapy (ICS/LAMA/LABA) improves lung function, symptoms, and exacerbations more than either ICS/LABA or LABA/LAMA

(a) Any arm with ICS (both ICS/LABA and triple therapy) had increased risk of PNA

130
Q

Benefit of roflumilast in COPD chronic bronchitis w/ exacerbations

A

Reduced exacerbations, modest improvement in lung function

Not improved mortality

REACT trial, Lancet 2015

131
Q

Describe GOLD group C COPD

(a) First line treatment

A

GOLD C

(a) LAMA or LAMA/LABA combo

132
Q

Describe GOLD group A

(a) First line treatment

A

GOLD group A: low symptoms and low exacerbation risk

(a) SABA PRN

133
Q

Describe GOLD group B

(a) First line treatment

A

GOLD B- bottom R of 2x2
High symptoms but low exacerabtions (under two in the past year and no hospitalization)

(a) Tx- LAMA (spiriva) or combo LABA/LAMA

134
Q

Things that reduce mortality in COPD

A

-smoking cessation
-long term oxygen therapy for PaO2 under 55 or SpO2 under 88 at rest
-noninvasive ventilation for GOLD class IV and pCO2 over 45, pH over 7.35 (so chronically compensated)

Things that don’t: all the inhaled and oral meds, pulmonary rehab

135
Q

Treatment for alpha-1 antitrypsin

(a) Inhalers?
(b) Indications for replacement

A

Alpha-1 Antitrypsin
-autosomal dom
-ZZ, null

(a) Same inhalers based on obstruction level in COPD, use to control symptoms
(b) Exogeneous alpha-1 protein by pooled human given weekly for:
-AAT levels below critical threshold of 11 umol/L

136
Q

Most common cause of viral exacerbation of COPD

A

Rhinovirus

Influenza in ICU, but not overall

137
Q

Subgroup with most definitive mortality reduction with lung volume reduction surgery

A

Upper lobe heterogeneous emphysema with low baseline exercise capacity

138
Q

Describe the tram-track sig of bronchiectasis

(a) In cross section is what sign?

A

Lack of tapering as airway extends distally

(a) Signet ring sign

139
Q

Kartagener’s syndrome in primary ciliary dyskinesia

A

Kartagener’s syndrome triad:
rhinosinusitis
bronchiectasis
situs inversus (heart on R, liver on L)

140
Q

Differentiate class mutation of F508D and G551D for CF mutations

A

F508D- class II mutation, abnormal transport to cell membrane

G551D- class III mutation, abnormal regulation of function so inhibited chloride channel activation (but channel gets to cell membrane ok)

141
Q

Explain direct consequence on electrolyte imbalance due to defective CFTR in respiratory epithelium

A

Defective CFTR (either doesn’t get to cell membrane, abnormal regulation etc)- Cl cant get out of cell, too much Na (and therefore water) gets into cell

Na/water into cell => decreased viscosity of mucus layer

142
Q

How to confirm CF diagnosis if positive IRT (immunoreactive trypsinogen) screening in newborn

A

Positive screening test, have to check sweat chloride test

Definitive diagnosis if sweat chloride over 60 mmol/L on two tests

Unlikely test if sweat chloride under 29 mmol/L

30-59: test for CFTR mutation allele, c/w diagnosis of 2 mutations. If 0 or 1 mutation- repeat sweat chloride or send expanded DNA analysis

143
Q

Differentiate effect of exocrine vs. endocrine pancreatic insufficiency in CF

A

Pancreatic insufficiency

endocrine => diabetes

exocrine => ingestion specifically of fat due to lack of pancreatic enzymes => replace with ADEK (fat soluble) vitamins

144
Q

Put in order inhaled therapies for CF patients over the age of 6 years old

A
  1. Inhaled bronchodilator
  2. Hypertonic saline (3 or 7%)
  3. Dornase alpha (inhaled DNase)
  4. Airway clearance (chest vest, aerobika)
  5. Inhaled antibiotics if colonized with pseudomonas
145
Q

Mechanism of dornase alpha

(a) Indication for CF pts

A

Dornase alpha = inhaled DNase, breaks down extracellular denatured DNA released by degenerating neutrophils

(a) All CF patients over 6 yers of age to thin mucus

146
Q

Indication for aerosolized antibiotics in CF patients

A

Inhaled aztreonam or tobramycin in CF pts over 6 y/o colonized with pseudomonas (see on surveillance cultures every 3 months)

147
Q

How to diagnosed primary ciliary dyskinesia

A

Nasal biopsy with electron microscopic examination of cilia

148
Q

Mechanism of ivacaftor

(a) For which mutation

A

Ivacaftor = potentiates activity once on cell membrane
-doesn’t help much for F508D b/c class II mutation with difficulty getting to cell membrane
-does help with class III where abnormal regulation/activity on cell surface

(a) G551 mutaion

149
Q

Asthma Pathophys

(a) What secretes IgE
(b) Function of IgE
(c) Cytokine specific for eosinophils

A

(a) B cells release IgE
-B cells stimualted by IL4/IL-13 released from Th2 cells

(c) IgE then activates mast cells and basophils => degranulation

(c) IL-5 specific for eosinophil maturation and survival

150
Q

Differentiate functions of IL-4 and IL-13

A

Both IL-4 and IL-13 work on class switching to promote B-cells to release IgE

Then IL-13 also works on airway smooth muscle to mediate hyperresopnsiveness and mucus hypersecretion

151
Q

Cytokine that mediates class switching of B-cells to release IgE

A

Both IL-4 and IL-13 mediate class switching

152
Q

Type 2 vs. non-T2 asthma

(a) Main cytokines involved
(b) Main cells involved

A

T2 asthma
(a) IL-4, IL-5, IL-13
(b) Eosinophils, Th2

Non-type2 asthma
(a) IL-8, TNF, IFN
(b) Neutrophils

153
Q

Cutoffs for type-2 biomarkers in asthma

Low, medium, high of

(a) Total IgE
(b) Blood eosinophils
(c) FeNO

A

Type 2 asthma biomarkers

(a) Total IgE: low under 30, moderate 31-149, high over 150

(b) Blood Eos: low under 150, medium 150-99, high over 400

(c) FeNO: low under 25 ppm, medium 26-49, high over 50

154
Q

What is the sputum eos cutoff consider significant for T2 asthma?

A

Sputum eos 3 or above % considered high

155
Q

FeNO

(a) Exhaled levels higher or lower in asthmatics?
(b) Changes to steroids?
(c) Cofounders

A

FeNO

(a) Higher levels in asthmatics, thought that eosinophilic inflammation triggers NO release => noninvasive marker of airway inflammation
(b) FeNO typically normalizes with steroid tx
(c) Age, smoking status, medications, steroid use (duh)

156
Q

FeNO

(a) Exhaled levels higher or lower in asthmatics?
(b) Changes to steroids?
(c) Cofounders

A

FeNO

(a) Higher levels in asthmatics, thought that eosinophilic inflammation triggers NO release => noninvasive marker of airway inflammation
(b) FeNO typically normalizes with steroid tx
(c) Age, smoking status, medications, steroid use (duh)

157
Q

Differentiate direct vs. indirect bronchoprovocation testing

(a) Methacholine is which one?
(b) Which has better sensitivity vs. specificity?
(c) FEV1 cutoff as positive

A

Direct- substance that directly causes bronchoconstriction
(a) Methacholine = direct
(b) Good sensitivity, negative methacholine challenge in a symptomatic pt rules out asthma
(c) Greater than 20% drop in 20% is positive

vs.

Indirect- typically dries out mucosal surface to cause bronchoreactivity
ex: exercise induced, hypertonic saline, mannitol, allergens
(b) Indirect- more specific, less sensitive
(c) Testing continues until 15% drop in FEV1 from baseline (lower cutoff than direct b/c of mechanism) ex: mannitol used in SEEK question

158
Q

Describe steps of methacholine challenge and the PD20

A

Give escalating doses of nebulized methacholine with spirometry after each dose, stop the test when FEV1 drops to 20% of baseline
-dose of methacholine required to cause 20% drop in FEV1 = PD20, correlates with degree of airway hyperreactivity

159
Q

Cutoff PD20 for a positive methacholine test

A

PD20 under 100 considered positive, under 25 is moderate
100-400 = borderline
25-100 = mild

Lower dose of methacholine required to drop FEV1 by 20% correlates with more severe airway hyperresponsiveness

160
Q

Differentiate asthma severity and control

A

Severity marked by degree of medications required to achieve good control

vs.

Control- controlled, poorly controlled, uncontrolled- degree to which current treatment controls symptoms and reduces impairment/risk

161
Q

Comparing step-up treatment for asthma vs. COPD

(a) ICS use
(b) LAMA monotherapy

A

Asthma vs. COPD

(a) ICS earlier in asthma- included PRN in step 2 and ICS-LABA standing in step 3
(b) LAMA monotherapy not recommended in asthma, but used for GOLD B or C in COPD

162
Q

Mechanism of montelukast

(a) Benefit vs. placebo
(b) Benefit vs. ICS
(c) 2 cases when specifically to consider early in treatment

A

Montelukast = leukotrene receptor blocker

(a) Reduces exacerbations, improves symptoms
(b) Modest benefit, less than ICS
(c) Consider earlier in aspirin-exacerbated respiratory disease and exercise-induced bronchoconstriction

163
Q

Name the asthma biologic with the following mechanism:

(a) Anti-IgE
(b) Anti-IL-5
(c) Anti-IL4Ra
(d) Anti-IL5R

A

Asthma biologic

(a) Anti-IgE = omalizumab (xolair)
(b) Anti-IL-5 = mepolizumab (nucala)
(c) Anti-IL4Ra = dupilumab (duplixent)
(c) Anti-IL-5R = benralizumab (fosenra)

164
Q

Indications for omalizumab

A

Moderate-severe allergic asthma
-IgE level 30-700 AND allergen-sepcific IgE to perennial (year-long, not seasonal) allergen

165
Q

Differentiate indications for mepolizumab and benralizumab

A

Mepolizumab (anti-IL5) and benralizumab (anti-IL5R) both for severe eosinophilic asthma (serum eos over 150)

-mepolizumab also FDA approved for EGPA

166
Q

Which asthma biologic is first line for the following comorbidities?

(a) Atopic dermatitis
(b) EGPA
(c) Nasal polyposis

A

Biologic based on comorbidity

(a) Atopic dermatitis- dupilumab (anti-IL4Ra)
(b) EGPA- mepolizumab (anti-IL5)
(c) Nasal polyposis- dupilumab anti-IL4Ra)

167
Q

Which asthma biologic to use for oral corticosteroid dependent asthma w/ normal eos level

A

3 separate biologics are approved for oral corticosteroid dependent asthma: mepolizuab (anti-IL5), benralizumab (anti-IL5R), and dupilumab (anti-IL4Ra) but only dupilumab independent of eos level

so steroid dependent w/o elevated eos (eos under 150)- use dupilumab (anti-IL4Ra)

168
Q

Discuss flow/algorithm for choosing an asthma biologic in patients on oral prednisone

A
  1. Of course confirm diagnosis, inhaler technique, compliance etc and maximize inhaled medications
  2. Severe asthma with vs. without oral glucocorticoid use, both go split by eos count
    -OCS needed: then split by eos count
    –Eos not elevated in last 12 months = Anti-IL4Ra (dupilumab)
    –Eos elevated in last 12 months- have a choice of anti-IL4Ra (dupilumab), anti-IL5 (mepolizumab, nucala), or anti-IL-5Ra (benralizumab, fosenra)

Then taper oral pred gradually and assess response

169
Q

Discuss flow/algorithm for choosing an asthma biologic in patients not requiring oral prednisone

A
  1. Of course confirm diagnosis, inhaler technique, compliance etc and maximize inhaled medications
  2. Severe asthma with vs. without oral glucocorticoid use
170
Q

Typical biomarker cutoff for the following asthma biologics

(a) Omalizumab
(b) Mepolizumab

A

(a) Omalizumab (Xolair) IgE 30-700
(and allergen-specific IgE to perennial allergen)
(b) Mepolizumab (nucala, anti IL-5) typically requires serum eos over 150 in the past 12 months

171
Q

Bronchothermoplasty

(a) How it works
(b) Benefit

A

Bronchothermoplasty

(a) Reduce smooth muscle mass
(b) Reduces exacerbations, no mortality change (AIR2 trial)

172
Q

2 indications for ASA desensitization in patients with aspirin-exacerbated respiratory disease

A

Desensitization to ASA if:

  1. severe, refractory nasal polyposis
  2. another strong indication requiring ASA therapy (ex: PCI)

-desensitize then have to continue daily ASA

173
Q

Exercise-induced bronchoconstriction

(a) proposed mechanism
(b) gold standard for diagnostic testing
(c) tx

A

Exercise-induced asthma

(a) Large volume cold air triggering airway hyperreactivity
(b) Indirect bronchoprovocation test, exercise challenge test
-positive if 15% reduction in FEV1
(c) Start with pre-treatment of SABA, can add ICS/LABA if needed

174
Q

Main clinical benefits of asthma biologics

A

Really the 50% reduction in exacerbations, then also reduction in oral corticosteroid use

-typically FEV1 improvements are present but don’t always meet MCID

175
Q

Ideal COPD pt candidate for initiation of long-term nocturnal noninvasive?

A

Chronic, stable COPD 2-4 weeks following discharge (so not upon discharge from hospital) for acute exacerbation of COPD with compensated hypercapnia (pCO2 over 45, pH over 7.35) after which OSA is already ruled out

-so not patient in hospital pending discharge, pending PSG, or worsening symptoms

176
Q

2 groups for which long-term O2 therapy improves survival

A
  1. Resting hypoxia: PaO2 under 55 or SpO2 under 88% at rest
  2. PaCO2 56-59 with e/o polycythemia or cor pulmonale

–not those w/ exercise desat (LOTT trial) showed no sig difference in death, first hospitalization, or exacerbations

177
Q

52M with frequent COPD exacerbations, negative alpha-1 antitrypsin, FEV1 21%. No cough or sputum. On high-dose LAMA/LABA

Next best step: triple therapy or add azithro?

A

First upgrade to triple therapy, thennn add azithro
-don’t be confused by tons of exacerbations, maintenance macrolide added to triple therapy

178
Q

Describe how brensocatib (oral inhibitor of dipeptidyl peptidase 1) may work to reduce exacerbations in non-CF bronchiectasis

A

Works to reduce neutrophil serine protein activity

-DPP1 activates neutrophil serine protease enzymes (ex: neutrophil elastase) that are elevated in non-CF bronchiectasis (typically high neutrophils => IL-8 overexpression)

179
Q

69M with COPD- former 1/2 PPD smoker x30 years. Symptoms controlled on LAMA, FEV1 68%

Next best test for COPD mgmt?

A

Trick question (eye-roll): doesn’t meet criteria for lung CA screening b/c under 20 pack years (current criteria: 50-80 yoa with at least 20 pack year history quit within last 15 years

Next best step- bone densitometry given high risk of osteoporosis

180
Q

Bronchial atresia

(a) Pathogenesis
(b) MC affected lobe
(c) MC typical presentation
(d) Imaging finding

A

Bronchial atresia

(a) Congenital anomaly where airway doesn’t form
(b) Most commonly apicoposterior segment of LUL
(c) Typically asymptomatic, but can present w/ infection and air trapping
(d) Mucoid impaction at atretic area and distal hyperinflation

181
Q

34F with CF with chronic cough unchanged from baseline p/w stable FEV1, surveillance Cx grows pseudomonas- next step?

A

Inhaled tobramycin x28 days

-not IV abx given asymptomatic, can used inhaled to try to eradicate for initial pseudomonas infection
-definitely don’t ignore, treatment of early pseudomonas leads to more sustained eradication, less overall abx use (though no clear benefit in mortality, rate of lung fxn decline, or mortality

182
Q

20M poorly controlled asthma despite adherence to triple therapy inhaler and montelukast. Normal eos, normal IgE, no atopy, on low dose oral steroids for 6 months with persistent daily use of albuterol

Which mab is indicated?

A

Dupilumab (anti-IL4R)- effective as add-on maintenance for oral corticosteroid-dependent asthma regardless of phenotype

-not omalizumab (anti-IgE) b/c IgE levels 30-700 required
-mepolizumab and reslizumab (anti-IL5s) approved for add-ons for oral steroid-requiring asthma ONLY if pt has elevated eos count (over 150 for mepolizumab, over 400 for reslizumab)

183
Q

Exclusion criteria for bronchial thermoplasty study

(a) number of exacerbations
(b) FEV1
(c) Good response to prior bronchial thermoplasty
(d) Asthma control

A

Bronchial thermoplasty to reduce large/medium airway smooth muscle mass

(a) Excluded pts with more than 3 exacerbations in the past year
(b) Excluded for FEV1 under 60%
(c) Excluded if had prior bronchial thermoplasty (so evidence of prior partial response is irrelevant)
(d) Need poor asthma control (ora steroid use) but in a chronic state at time of procedure

184
Q

Most common adverse effect of endobronchial valve insertion

A

Pneumothorax in 25% in the first month, highest risk in first 3 days

CM Pulmonary Boards (11 decks)

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