Respiratory System Pathology 4 - Galbraith Flashcards by Autumn Brubaker

Defense mechanisms in the lung compromised in infections

Cough reflex
Impaired or diminished ciliary function
Mucus stasis
Decreased macrophage activity
Pulmonary edema

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Community-acquired bacterial pneumonia (CAP)

CRP and procalcitonin levels higher in bacterial pneumonia

May follow viral URI

Predisposing conditions:
Young or old
COPD, DM, CHF
Absent splenic function - encapsulated bacterial infections

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Streptococcus pneumoniae

most common cause of CAP
Gram +
Elongated diplococci
Seen in sputum
*false positives

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Haemophilus influenzae

cause of CAP
Gram -
encapsulated type b most virulent
pediatric bacterial pneumonia, OM
most common cause of bacterial acute exacerbation of COPD

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Moraxella catarrhalis

cause of CAP
Elderly: bacterial pneumonia, exacerbation of COPD

Pediatric: OM

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Staphylococcus aureus

cause of CAP
secondary bacterial pneumonia following viral

higher incidence of complications - abscess, empyema

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Klebsiella pneumoniae

cause of CAP
Gram - bacterial pneumonia
chronic alcoholics, malnourished

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Pseudomonas aeruginosa

cause of CAP
pneumonia in CF, neutropenic
Hematogenous spread

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Legionella pneumophila

cause of CAP
water tanks, pipes
Immunosuppressed, chronic disease
Urine Legionella antigen

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Mycoplasma pneumoniae

cause of CAP

children, young adults

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pneumonia morphology

alveolar filling with inflammatory cells and exudate
–> consolidation (solidification) of lung tissue

Patterns:
bronchopneumonia
Lobar pneumonia

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Bronchopneumonia morphology

patchy involvement of lung parenchyma
Consolidated areas may coalesce
Formed of acute suppuration
Basal, often mutlilobar and frequently bilateral

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Lobar pneumonia morphology

consolidation of an entire lobe

Stages:
Congestion - vascular engorgement, cell-poor intra-alveolar fluid with bacteria
Red hepatization - robust exudate with neutrophils, erythrocytes, fibrin
Grey hepatization - fibrinosuppurative material, erythrocyte disintegration, early organization
Resolution - organizing fibrosis admixed with macrophages

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Clinical course of CAP

Abrupt fever, shaking chills, productive cough - rust colored sputum

Lobar: CXR opaque lobe
Bronchopneumonia: CXR focal opacities

Abx: culture and sensitivity

Complications:
Abscess
Empyema - pleural involvement
Bacteremia

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Community acquired Viral pneumonia - organisms, predisposing factors

Influenza A, B, C
RSV
Human metapneumovirus
Adenovirus
rhinoviruses

Predisposing factors:
Very young, elderly
Malnutrition/alcoholism
Chronic disease

Inflammation and damage to ciliary mechanism –> bacterial superinfection

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Influenza A virus

Virus virulence factors (Ab response targets):
Hemagglutinin (H1-H3) bind to respiratory epithelial cells allowing cellular infection

Neuraminidase (N1-N2) - allows release of newly created virions

Genome: 8 RNA segments

Viral RNA polymerase lacks error detection –> antigenic drift

Recombination of segment genome when connected with different types
-antigenic shift leading to new strain –> pandemic

Influenza virus infection morphology

Upper respiratory tract
Infects respiratory epithelium causing:
-Intraalveolar fluid accumulation
-cell death
-inflammation

Lung infection patchy or extensive

Vascular congestion
Inflammation in alveolar wall interstitial tissue
-edema
-lymphocytes and macrophages

Influenza virus clinical course

variable

Extent of disease affected by:

Host immune status
Virulence of strain
presence/absence of other complicating conditions

Histoplasma capsulatum

intracellular fungal pathogen
Inhaled soil particles contaminated with bird/bat droppings

US: endemic along Mississippi and Ohio rivers - much of the Midwest

Targets macrophages

Histoplasmosis clinical course

Self-limited pulmonary infection

Chronic, progressive lung infection

apical
night sweats, fever, coughing

extra pulmonary involvement
-liver, adrenal glands, mediastinum, meninges

wide dissemination

Histoplasmosis morphology

Granulomas - often caseating

May coalesce and consolidate lung focally or form cavities

resolve and form nodular calcified scars

Silver stain: 3-5 um yeast

Disseminated disease: within clusters of macrophages, caveating granulomas not seen

Blastomyces dermatiditis

soil dwelling dimorphic fungus

Central and Southern US

In tissue form 5-15 um yeast with double wall and visible nucleus

Broad Based Budding

Forms granulomas with superimposed suppuration

May resolve spontaneously

Pulmonary blastomycosis

productive cough, chest pain
headache
Anorexia, weight loss, fever, chills, night sweats

Coccidioides immitis

Southwest US

Infective form - arthroconidia which are inhaled

Taken up by macrophages - resist intracellular killing

Lung granulomas - giant cells containing large spherules (20-60um) filled with endospores

Rupture of spherules may induce recruitment of neutorphils

Coccidiomycosis

subclinical and self limiting Minority: San Joaquin Valley Fever -fever, cough, detectable lung granulomas, pleuritic pain, skin lesions - erythema nodosum, erythema multiforme

Etiologic factors and incidence of lung carcinomas

Most between 40-70 yo, peak 50s-60s Smoking: - direct relationship between cancer frequency and pack-year history - genetically susceptible to tobacco smoke - polymorphisms of CYP450 mono-oxygenase Environmental exposure: -Asbestos, uranium, vinyl chloride

Squamous cell carcinoma

Strong association with tobacco smoke p53 mutations and over expression preceded in bronchial epithelium by squamous metaplasia, dysplasia, CIS Often arise in central lung/hilar region

Adenocarcinoma

Smokers or nonsmokers likely peripheral Gain of function mutations: EGFR, ALK, ROS, MET, RET, KRAS Precursor lesions: - atypical adenomatous hyperplasia (less than or = 5mm) - adenocarcinoma in situ (less than 3 cm) - cells are more atypical and may be mutinous Invasive positive TTF-1 staining for lung origin (primary site, rather than mets)

Small cell carcinoma

Strongest association with smoking TP53 and RB mutations Aggressive, very high fatality rate Central or peripheral, likely from neuroendocrine cells in bronchial epithelium -Immunostains for chromogranin, synpatophysin, CD57+ Tumor cells small, little cytoplasm, closely arranged with "molding" and absent nuclei Cells grow in clusters without architectural pattern Marked necrosis

Metastatic carcinoma of lung

Any type of lung CA may spread to pleural space Spread hematogenously or within lymphatics -mediastinal, bronchial, paratracheal nodes Mets to: Adrenal glands, liver, brain, bone

Carcinoid tumor

arise from bronchial neuroendocrine cells -neuroendocrine tumorlets, carcinoid tumors, small cell carcinoma under 40 yo Low grade malignant neoplasm - typical and atypical forms

carcinoid tumor morphology

central or peripheral -central carcinoids protrude into bronchial lumen organoid Nexus of regular cells -moderately abundant cytoplasm and regular round nuclei Atypical carcinoids show cell variability and higher mitotic activity -invade lymphatic vessels

Carcinoid tumor clinical course

symptoms related to bronchial obstruction -coughing, hemoptysis, impaired drainage Carcinoid syndrome - tumors secreting vasoactive amines (serotonin): Flushing Diarrhea Cyanosis 95% 5 year survival for typical carcinoids 70% for atypicals

Tumors metastatic TO the lung

most common site of tumor mets via blood or lymphatics Growth pattern is multiple, scattered nodules Common primary sites: Breast, colon, kidney, prostate, urinary bladder

Malignant mesothelioma

asbestos exposure NOT compounded by smoking homozygous deletion of p16 arises in visceral or parietal pleura, spreads to pleural space --> ensheathing and compressing lung May invade adjacent thoracic structures

Malignant mesothelioma morphology and course

epithelioid and sarcomatoid types IHC differentiates MM from adenocarcinoma Present with CP, dyspnea, recurrent pleural effusions Concurrent asbestos-related interstitial fibrosis 1 yr survival 50%, most do not survive 2 years