Lung Path, Infxn, Resp Symptoms and Bio Flashcards
Which airways have cartilage vs. don’t?
Presence of cartilage differentiates bronchus (present, to maintain patency) from bronchioles (cartilage disappears)
Differentiate bronchus from bronchiole
Bronchus has cartilage to maintain patency, bronchiole defined by lack of cartilage
-bronchiole in bronchovascular bundle same size as adjacent PA branch
Differentiate two types of bronchioles
Bronchioles = airways w/o cartilage (vs. bronchus w/ cartilage)
- membraneous bronchiole = continuous muscular wall, then gives rise to respiratory bronchiole
- respiratory bronchiole = partial muscular with partially alveolated wall
- then respiratory bronchiole gives rise to alveolar duct (completely alveolar wall)
Anatomically define alveoli
Alveoli = blind ending sacs that are the site of gas transfer, alveoli coalesce to form alveolar ducts –> respiratory bronchioles (partially muscular, pratially lined w/ alveoli) –> membranous bronchioles (all muscular not lined w/ alveoli)
Define lobule
Lobule = lung parenchyma sitting between two interlobular septa
-picture showing respiratory brochiole and PA artery branch
Immunohistochemical features differentiating the three most common types of lung CA
Squamous: p40+, TTF-1 negative
Adeno: TTF-1 positive, p40 negative
Small cell: combo: TTF1 positive, CD56/chromogranin, synaptophysin positive (so TTF-1 positive doesn’t differentiate adeno and small cell, need cell morphology)
Pulmonary carcinoid tumors
(a) Typical location
(b) Pathologic findings
(c) Why can’t cure with curetting?
Pulmonary carcinoid- all malignant
(a) Typically endobronchial
(b) Highly vascular, then grade with mitotic figures and degree of necrosis
(c) Have to resect, can’t just curette out, b/c always invade the bronchial wall
Most common etiology of imaging finding
Hamartoma- benign solitary pulmonary nodule with characteristic popcorn calcification
-typically fat, calcification
Most likely which lung cancer given finding of intercellular bridge?
Finding seen in squamous cell carcinoma
- keratinization (squamous pearls) and/or intercellular bridges
- p40 positive, TTF-1 negative
Histologic features (not stains) that differentiate squamous cell carcinoma from adenocarcinoma
Squamous cell- keratinized cells, intercellular bridges
AdenoCA- makes glands or secretes PAS+ mucin
What is lepidic growth?
(a) Characteristic of what malignancy?
Lepidic growth = growing along alveolar walls
(a) Adenocarcinoma in situ (AIS, new name for BAC) start with lepidic growth (thickened-appearing alveoli with atypical cells). AIC grows in uniform manner along alveolar walls w/o evidence of invasion
Histologically differentiate minimally invasive adenoCA from lepidic predominant adenoCA
Both have background of peripheral lepidic growth, then different size of invasive part
- minimally invasive aenoCA: lepidic growth background with under 5mm invasive part
- lepidic-predominant adenoCA: lepidic growth background with invasion over 5mm
Why clinically relevant to see if lepidic growth has any areas of invasion?
If no invasion then adenocarcinoma in situ (AIS, formerly called BAC) is 100% curable with local wedge resection
- pure lepidic growth = AIS
- once have any area of invasion: if under 5mm = minimally invasive adenoCA, if over 5mm = lepidic predominant adenoCA
Which lung nodule is more concerning?
Left = pure GGO- presume adenocarcinoma in situ (AIS, BAC) or minimally invasive adenoCA (invasive component under 5mm) = better prognosis
vs.
Larger the solid component = higher risk of invasion, if over 50% solid or growing solid component higher concern for lepidic predominant adenoCA
How is adenocarcinoma characterized?
(a) Why clinically relevant
Not characterized by well or poorly differentiated, instead based on histologic subtype
- High grade = solid and micropapillary
- Intermediate grade = acinar and papillary
(a) Relevant b/c high grade (solid and micropapillary) have worse prognosis than intermediate (acinar and papillary)
Differentiate WHO 2015 classification of squamous cell and adenocarcinoma
WHO 2015 classification
- squamous cell = keratinizing (cells that make keratin) or p40 positive
- adenocarcinoma = diffusely TTF-1 positive whether they make glands or contain mucin (b/c not all do, cann be poorly differentiated and just have the stain)
What is the most likely lung malignancy given this histology?
Small cell- 2-3 x number of lymphocytes (small cells), then very blue b/c high nuclear (blue) to cytoplasmic ratio
Defining features of large cell carcinoma
- large cells (specifically large nucleoli) notably WITHOUT features of squamous (keratinic, intercellular bridges) or adenocarcinoma/glandular (mucinous, papillary) differentiation
- negative p40 (squamous) and TTF-1 (adenoCA)
Why important clinically to separate adenoCA and squamous cell CA
Yes both are NSCLC so have the same staging and similar treatment algorithms
-but adenoCA more likely to have EGFR, VEGF, ALK/ROS mutations while squamous do not => immunotherapy
How to histologically define the size of adenocarcinoma vs. adenocarincoma in situ
Adenocarcinoma tumor size counted by the INVASIVE portion of the lesion, not the entire lesion
-can have lepidic growth but the tumor size is based on the invasive portion
How are pulmonary carcinoid tumors classified?
Two types
- typical: less than 2 mitosis per 10 high power fields, absence of necrosis
- atypical (worse prognosis): 2 or more mitosis per 10 HPFs or presence of necrosis
Pulmonary carcinoid tumors
(a) Typical clinical features
(b) Smokers or nonsmokers
Carcinoid
(a) 70% are in proximal airways => cause airway symptoms like cough, hemoptysis, bronchial obstruction
(b) Typically in never smokers
2 malignancies with clasically false negative PET
- Adenocarcinoma in situ- ground glass nodule on imaging, low PET uptake
- pulmonary carcinoid tumors- typically in proximal airways
Differentiate management of pulmonary carcinoid tumors from other NSCLC
Pulmonary carcinoid- no proven benefit of chemo or radiation even for metastatic disease => just surgery and LN dissection even in most extensive form
- typical carcinoid (low mitoses, no necrosis): limited resection with segementectomy and regional LN dissection
- atypical sarcoid (more than 2 mitoses per 10 HPF or presence of necrosis): lobectomy and mediastinal LN dissection
Differentiate centrilobular from centriacinar
(a) Definition
(b) Histopath
(c) Radiology
(a) Lobule- between interlobular septa, made up of 5-15 acini (smallest unit of the lung)
(b, c) Histopath and radiology- too small to differentiate, so centrilobular = centriacinar
Centrilobular vs. panacinar emphysema
(a) Anatomic difference
(b) Typical risk factor
(c) Predominant location
Centrilobular emphysema
(a) hole in the center of the lobule with normal surrounding lung
(b) Smoking
(c) Upper-lobe predominant
Panacinar emphysema
(a) hole throughout entire lobule
(b) most common smoking but classically alpha-1 antitrypsin deficiency
(c) Lower lobe predomainant
Define paraseptal emphysema
Hole/dilated/destroyed distal alveoli lying perpendicular to the pleura- hence why seen in periphery on imaging
Typical histologic findings of asthma
Histologic features of asthma
- thickened basement membrane
- increased airway smooth muscle
- eosinophils in airway walls and lumen
2 key histologic features of smoking-induced respiratory bronchiolitis
- remodeling of small airway basement membrane so becomes thicker => narrowed lumen => obstructed flow
- smoker’s macrophages = hemosiderin-laiden macrophages, fill the lumen of the respiratory bronchioles causing turbulent flow
Infectious bronchiolitis
(a) Imaging finding
(b) Histopath finding
Infectious bronchiolitis
(a) Tree-in-bud opacities on CT chest
(b) Histopath: inflammatory cells (PMNs) in airwy wall and airway luemn
Differentiate bronchiolitis obliterans syndrome from constrictive bronchiolitis
BOS = syndrome of obstructed airways (FEV1 reduction) indicative of chronic rejection of lung transplant, the clinical syndrome
While constrictive bronchiolitis is the histopath equivalent
Pt with solitary lung nodule and this path from a core needle biopsy: diagnosis?
Malignant in adenoCA spectrum but cannot differentiate adenocarcinoma in situ (AIS, previously known as BAC, curable with wedge resection) from lepidic adenocarcinoma
-need complete excision to see if any invasive portion b/c tumor will be defined by size of invasive portion
Describe different histologic findings in early vs. late diffuse alveolar damage
DAD = pathologic finding of ARDS/AIP (AIP if idiopathic)
- first week = acute exudative phase with edema and hyaline membranes
- second week = proliferative/organizing stage with interstitial inflammation and organization (granulation tissue)
Diagnosis?
Hyaline membranes = in early/exudative phase of diffuse alveolar damage pathognomonic for AIP/ARDS
Histologic findings that differentiate early/late ARDS with pictures
- Early = exudative phase with hyaline membranes
- Late = organizing phase with collapsed parenchyma filled with granulation tissue
Histopath findings of organizing PNA
Organizing PNA pattern
- intra-alveolar buds of granulation tissue = granulation tissue inside respiratory bronchioles/small distal airways
- temporal homogeneity (all lesions of similar age)
- NO architectural distortion or old fibrosis (suggests another process)
Gross pathologic findings of UIP
Peripheral and lower lobe predominant fibrosis, thickened fibrotic walls grossly = pathologic equivalent of honeycombing
Histologic findings of UIP
- patchy fibrosis = abrupt fibrosis around the periphery just next to normal tissue = hallmark temporal heterogeneity
- newly created airspace with thick fibrotic wall = honeycombing, peripheral and lower lobe predominant
- **fibroblastic foci = tufts of granulation tissue tightly attached to lungs
Histopath buzzwords
(a) Fibroblast foci
(b) Hyaline membranes
(c) Basement membrane thickening with muscular hyperplasia
(d) Lepidic growth
(e) Stellate lesions
Histhopath buzzwords
(a) Fibroblast foci = granulation tissue tightly adherent to lung that fibrosis, = UIP
(b) Hyaline membranes = exudative phase of DAD (AIP/ARDS)
(c) Asthma
(d) Lepidic growth = along septa, seen in lung adenocarcinoma
(e) Lymphocytic infiltrate with stellate scars = PLCH
Describe histopath findings of progression of UIP
Fibrotblast foci = tufts of granulation tissue tightly attached to lung = site of injury and fibrosis
-characterized by dome-shaped fibroblastic tissue over collagen fibrosis
As disease progresses: foci get thicker, fibrosis gets denser, fibrosis geadually added to underlying lung (while etiology of non-steroid responsive granulation tissue remains unknwon)
Histologic description of acute IPF exacerbation
Expect UIP pattern (fibroblastic foci, peripheral and lower lobe predominant fibrosis with honeycombing) with DAD superimposed during acute exacerbation
-DAD features: hyaline membranes
What features on biopsy of UIP would suggest underlying CTD
(a) Why important clinically
UIP typically pauci-cellular => any lymhoid aggregates, plasma cells, or interstitial inflammation would suggest underlying ILD
(a) Start with immunosuppression (rather than anti-fibrotic) for tx and prognosis typically better in CTD-related
Differentiate imaging findings of cellular vs. fibrotic NSIP
NSIP radiographically: ground glass, subpleural sparing (vs. subpleural predominance in UIP), reticular opacities, traction bronchiectasis, NO honeycombing (cardinal feature of UIP)
- cellular NSIP on imaging: mostly ground glass
- fibrotic NSIP: start to see more reticular changes, typically subpleural sparing (not always present but when is helpful to differentiate from UIP)
Histopath features of NSIP
-temporal homogeneity (all same), vs. heterogeneous (due to different stages of fibroblastic foci/fibrosis) typical of UIP
^homogenous b/c fibrosis laid down on original alveolar walls
-lack of architectural distortion (again b/c fibrosis starts on original alveolar walls)
Why clinically important to differentiate cellular vs. fibrotic NSIP
Cellular in theory much more responsive to steroids and fully reversible! the fibrosis part is typically not reversible
-cellular NSIP much better prognosis (similar to DIP and RBILD) where fibrotic NSIP has worse prognosis (almost but not as bad as UIP)
Describe when respiratory bronchiolitis becomes ILD
-histopath can be identical (smoker’s macrophages in alveoli causing small airway obstruction) but when there is clinical evidence of ILD (PFTs) without another reason for ILD then RB on path = RB-ILD diagnosis
Histopath findings of RB-ILD
-respiratory bronchiolitis = pigmented alveolar macrophages (‘smokers macrophages’) in and around respiratory bronchioles and surrounding alveoli
Imaging features of RB-ILD
CXR: bilateral fine reticular or reticulonodular opacities
CT: fine centrilobular nodules, bilateral patchy GGOs, more GGO think more DIP b/c more interstitial fibrosis
Differentiate RB-ILD and DIP on
(a) Imaging
(b) Histology
(a) Imaging- more ground glass and dense consolidation b/c of more fibrosis
(b) Still tons of airspace macrophages, more interstitial fibrosis in DIP
This CT chest in a smoker, dx?
Cigarette and MJ smoking associated cystic lung disease- centrilobular nodules with cysts = PLCH
-predominantly upper and mid lung zones
Histologic findings of PLCH
- early PLCH = cellular with tons of Langerhan cells (APCs, subtype of dendritic cells) characteristically stain + S-100 and CD1a
- then later on stellate and cellular nodules (of Langerhan cells) fibroe and form stellate scars
PLCH treatment options
- smoking cessation is key
- steroids for severe or progressive disease
- BRAF inhibitor if BRAF mutation present
- transplant
- monitor for PH
Differentiate histologic granuloma pattern of 2 ILDs characterized by granulomas
Both noncaseating granulomas, but way more diffuse in sarcoidosis
- subacute HP: granulomas typically sparse or not present at all, typically interstitial inflammatory infiltrate
- while in sarcoidosis granulomas make up the disease so are diffuse, no interstitial infiltrate
Differentiate comon etiologies of nonfibrotic vs. fibrotic HP
Nonfibrotic- high percent bird (including down pillowsbedding) and mold/humidifier exposure
Fibrotic (chronic)- mold/humidifier, idiopathic
Imaging findings of nonfibrotic HP
GGOs, centrilobular nodules with air trapping
Histopath findings of nonfibrotic HP
- interstitial inflammation ceneterd around bronchovascular bundles
- sparse granulomas
Imaging features to help differentiate chronic HP from UIP
Both can have honeycombing and fibrosis
- while HP more upper-lobe predominant with centrilobular nodules (not seen in UIP) and air trapping
- upper lobe predominant, honeycombing in both (red arrow) and more groun glass (white arrow) in HP
Histopath findings to help differentiate UIP from fibrotic (chronic) HP
Both can have peripheral fibrosis and honeycombing
-small granulomas in HP (not in UIP)
Why clinically important to differentiate chronic HP from UIP
Different treatment
UIP- straight to antifibrotic
Fibrotic HP- immunosuppression (steroids, AZA, MMF), then if still progressive add anti-fibrotic (INBUILD study)
Describe the histologic pathphysiology of scarring in sarcoidosis
Sarcoid- starts with noncaseating granulomas along the bronchovascular bundle, then develop concentric fibrosis around the granulomas, then eventually granulomas coalesce with fibrosis surroudning and all fibrosis
Diagnosis based on path
LAM = lymphangiomyomatosis
-mTOR pathway not inhibited (either from TSC mutation or abnormal signagling of mTOR) so get anormal cell proliferation/sruvival/invasiveness => pecular smooth muscle like cells then cysts form
Typical immunohistochemical markers of LAM
+HMB-35, ER and PR positive (but weirdly anti-estrogens don’t work)
Other organs involved in LAM
See LAM cells (abnormal smooth muscle cells) in chylous effusions, blood, angiomyolipomas of the kdney
Why does LAM often present with PTX?
B/c thin walled cysts in periphery at high risk of rupture => PTX
-cysts are very thin walled and peripheral
Differentiate etiologies of PAP
(a) Primary/acquired
(b) Congenital
(c) Secondary
PAP = accumulation of surfactant, normal physiology requires GM-CSF to activate macrophages to degrade surfactant
(a) Primary/acquired = development of anti-GM CSF antibodies
(b) Congenital = mutation in GM-CSF gene or receptor, or in surfactant protein so alveolar macrophage cannot degrade
(c) Secondary = something else wrong with macrophage that it can’t degrade surfactant
ex: immunocompromised pt w/o macrophages, drug reactions, exposures (acute silicosis)
Biopsy findings of PAP
-Periodic acid-Schiff-(PAS) positive alveolar deposits (surfactant) in absence of ecellular infiltrate and normal septa
BAL findings of PAP
(a) Electron microscopy
- return of milky effluent with granular, acellular, eosinophilic, proteinaceous materal with foamy macrophages
- confirmatory finding = lamellar bodies (concentrically laminated phospholipid structures) on electron microscopy
Biopsy findings of acute eosinophilic PNA
= DAD (hyaline membranes) + eos
Characteristic imaging features of chronic eosinophilic PNA
“photographic negative of pulmonary edema”
-dense peripheral consolidations, often migratory
Biopsy findings of chronic eosinophilic PNA
Just huge sheets of all eos
-similar to bacterial PNA but instead of neutrophils, all eos
Which organism?
V-shaped, 45 degree branchng on India ink or K-OH stain = aspergillus
Aspergillus vs. mucor?
Left = aspergillus- smaller angle branching, regular septations
Right = mucor- closer to 90 degree branching, wider, no regular septations
HIV pt with fever, cough, dyspnea, hemoptysis
- multiple nodules on CT chest
- pulmonary artery pseudoaneurysm
- tissue sample:
90 degree hyphal branching without septations and thick filaments = mucor
- more nodules (over 10) typically favor mucor over invasive pulmonary aspergillosis
- tissue necrosis and crossing of tissue planes/angioinvasiveness => PA microaneurysms/pseudoaneurysms
Differentiate histology of endemic mycoses
Histo- narrow-based budding yeast
Coccidio- giant sperhules with endospores
Blasto- broad-based (B’s) budding yeast
Paracoccidio- ‘pilot-wheel’ appearance of fungal elements
Diferentiate location of endemic mycoses
- Histo (more common) and blasto (less common) overlap with Ohio and Mississippi River Valleys- central and midW US
- Coccidiomycosis: more SW US, agriculture associated, Arizona
- Paracoccidio: S. America and Mexico
Buzzword india ink stain
(a) Diagnosis
India ink stain- positive in cryptococcus neoformans
(a) Classic halo sign of encapsulate yeast of cypto- typically of meningitis or pulmonary involvement
Pt with skin finding on face, chronic cough x3 months with following CT chest
(a) Dx
(b) Tx
(a) Dx- actinomyces, bacteria that causes pulmonary cavitation with chest wall/pleural involvement/invasiveness
- also typically cervicofacial involvement in otherwise immunocompetent
- air bronchograms in mass lesion with chest wall/pleural involvement
(b) Tx = PCN
Biopsy from an oral lesion in pt with cavitary lung disease
(a) Finding
(b) Diagnosis
(a) Sulfur granules = aggregates of actinomyces (branching, gram positive, thin filaments)
(b) Actinomyces- tx with PCN
Neutropenic patient with the following chest imaging and hemoptysis
(a) Dx
(b) Why hemoptysis
(c) First line tx
Halo sign of central infection with tissue invasion with surrounding blood, hyphae mold with septae and acute angle branching
(a) Invasive pulmonary aspergillus
(b) B/c known for its angioinvasion/characteristic vascular invasion, can spread hematogenously => small pulmonary infarcts (causing chest pain), hemoptysis
(c) First line tx for aspergillus = voriconazole
Treatment for bordatella pertussis
Azithro if caught within 1-2 weeks of symptom onset
Cough-variant asthma
(a) Gold standard confirmatory test
(b) First line tx
Cough-variant asthma
(a) Methacholine challenge test (direct bronchoprovocation test)
(b) First line tx = ICS
How long do symptoms persist after switching from ACEi to ARB for ACE-i induced cough
Symptoms typically resolve 1-4 weeks so doesn’t persist forever
Mucus buzzwords
(a) Malodorous
(b) Rust-colored
© Anchovy paste
(d) Caseous
Mucus buzzwords
(a) Malodorous- anaerobes
(b) Rust-colored = pneumococcus
© Anchovy paste, brownish, chocolate = ameobic lung abscess
(d) Caseous = tuberculsosi
Mucus buzzwords
(a) Chocolate/brownish
(b) Currant jelly sputum
© Barking cough sough
Mucus buzzwords
(a) Chocolate/brownish/anchovy paste = amoebic lung abscess
(b) Currant jelly = klebs PNA
© Barking cough think laryngotracheal infections = viral, diptheria, pertussis
34F previously healthy, non-productive cough 2 weeks after 2 days of myalgias, low grade fever, coryza
(a) Most likely dx
(b) First line tx
(a) Acute cough (under 3 weeks) most commonly post-viral
(b) Trial brompheniramine/pseudoephedrine combination = 1st gen antihistamine with decongestant
PAMPs (pathogen associate molecular patterns)- innate or adaptive immune response?
PAMPs = pathogen associated molecular patterns recognized by innate immune system to then stimulate inflammation and adaptive immune response
- innate immune response: immediate (faster), antigen independent, no immunologic memory
vs. slower adaptive immune response that is antigen dependent and provides immunologic memory
Innate or adaptive immunity?
(a) Alveolar macrophages
(b) Dendritic Cells
© T-cells
(a) Alveolar macrophages- innate immunity, antigen-independent immediate response w/o immunologic memory
(b) Dendritic cells = innate immunity
© T-cells = adaptive
Describe normal function of CTLA-4
Normally- CTLA-4 competes for co-stimulatory receptor on T-cells, so when CTLA-4 present it inhibits T-cell activation
Bad in cancer b/c the cancer develops CTLA-4 and then is not recognized as bad/foreign by immune system
ex: Anti-CTLA-4 blocks this receptor => blocks the inhibition so T cells remain active against the cancer cell
Mechanism of Ipilimumab vs. Pembrolizumab
Both CTLA-4 and PD-1 are receptors that work to inhibit T-cell response
Ipilumab = anti-CTLA-4 that blocks the inhibitory mechanism of CTLA-4 => T-cell remains active
Pembrolizumab = anti-PDL1 = blocks PD1 receptor to again prevent inhibition of T-cell
What has a better negative predictive value than MIP/MEP for ruling out respiratory muscle weakness?
Change in FVC from upright to supine
- normal to drop by 5-10%
- drop by 30% or more in FVC from upright to supine (higher when upright) has good negative predictive value for respiratory muscle weakness
FEV1 cutoff to not do methacholine challenge
Methacholine challenge
- absolutely contraindicated for FEV1 under 50% predicted or under 1L
- relative contraindication for FEV1 under 60% predicted or under 1.5L
Prior to methacholine challenge
(a) Which med to hold the longest
(b) How long to hold SABA
© How long to hold LABA
Prior to methacholine challenge
(a) Hold LAMA (tiotropium) for 48 hours
(b) No SABA morning of- 4-6 hrs
© Hold LABA 24-36 hrs
What percent drop in FEV1 is considered an abnormal exercise challenge test?
Decrease in FEV1 by 10-15% is abnormal
Explain the cutoff of back-extrapolated volume used in the acceptability criteria of PFTs
BEV (back extrapolated volume) must be under 5% of the FVC or within .1L, basically trying to ensure that when exhalation is started the lungs are full (not a lot of air has been exhaled)
-b/c if exhaled already then expiratory loop will be wrong
(from 2019 new ATS guidelines)
How close are PFT measurements (FEV1 and FVC) expected to be for acceptable reproducibility in the new 2019 ATS PFT guidelines?
Need 2-3 acceptable measurements within 0.15L of each other
Differentiate principle by which lung volumes are measured by body plethysmography vs. gas dilution
(a) Which is gold standard?
Body plethysmography (a) gold standard- pt pants against a closed shutter in a sealed box, then via Boyles law (P1V1 = P2V2) use the change in pressure to calculate the lung volume
Gas dilution- cheaper and easier- measure the concentration of exhaled gas (typically nitrogen washout) to calculate lung volume
Name two tracheobronchial abnormalities that classically spare the posterior membrane
(a) vs. which don’t
Spare posterior membrane:
- tracheobronchopathia osteochondroplastica = calcified nodules protruding into tracheal lumen but spares posterior membrane b/c no cartilage
- relapsing polychondritis = thickening of anterolateral wall, spares posterior membrane (again b/c no cartilage)
(a) Involve posterior wall: tracheal stenosis, tracheobronchomalacia, amyloid
What is this path trying to show?
Giant cells- activated macrophages fuse to form multinucleated giant cells in attempt to get rid of something (infection or foreign body)
Differentiate giant cell and granuloma
Giant cell = activated macrophages that fuse to try to get rid of either bacteria (Tb) or foreign body (ex: hard metal like cobolt)
Then if can’t get rid of the thing it calls for tons of inflammatory cells (lymphocytes, plasma cells, more macrophages) that form cuffs/swirls around the multinucleated giant cells to ‘wall off’
What is this path trying to show?
Giant cells- activated macrophages fuse to form multinucleated giant cells (abundant cytoplasm, multiple nuclei) in attempt to get rid of something (infection or foreign body)
-if can’t get rid of it then starts to form granuloma (big swirl of other cells around the multinucleated giant cell)
Differentiate the two types of granulomas?
Pt with progressive dyspnea 1 month after R-CHOP. Previously worked as a hay farmer. FEV1 22%, FVC 38%, ratio .45, DLCO 51%
Imaging and path below, diagnosis?
Constrictive bronchiolitis- airflow limitation due to small airway injury
Give away is the histology- airway itself is thickened (figure 7) leading to lumen obstruction
vs.
HP (figure 9 histology) where there is intraluminal fibrosis/endoluminal granulation tissue
Classic imaging finding for what diagnosis?
Reverse halo sign = atoll sign- crytogenic organizing PNA or fungal infections
-the patchy peribronchilar GGO make COP more likely
Classic imaging finding for what diagnosis?
Diffuse centrilobular ground glass nodules = subacute HP
