11-2: 12/8: Defense of the Lung Flash Cards

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Title: 11-2: 12/8: Defense of the Lung
Description: Matzer
Number of Cards: 41
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Author: bryant.faria9
Created: 2011-12-08
Tags: pulm
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    • Question
    • Answer
    • Side 3
    • Innate immunity of the lung
    • Anatomic filters, mucus, mucociliary excalator, epithelial lining of lung

      DOES NOT require prior infection or exposure
    • Describe how air flow (physically) changes from the trachea past the carina. How does this affect particle entrapment?
    • In the trachea, there's high velocity, laminar flow; high inertia of particles

      At carina (branch point), flow goes from laminar to turbulent. This allows for trapping of large air particles.

      Air flow then becomes lower velocity and laminar.
    • Ciliated _______ cells are found from the nose to the _______.
    • Ciliated pseudostratified columnar epithelium (and secretory cells) from nose to terminal bronchioles.
    • What is the epithelial cell type of the distal airways?
    • Cuboidal
    • How does injury/infection affect the airway lumen?

      What are the effects of this?
    • Injury/infection disrupts gap jns, tight jns and BM

      Leads to:
      1) leakage of proteins and cells into airway lumen-->inc'd mucous volume

      2) loss of polarity-->mucous composition no longer regulated

      3) loss of coordinated beating of cilia-->ineffective mucociliary clearance; due to Gap Jn damage (no coordination between cells)
    • Mucus:
      Function
      Components
    • Fns:
      Simple barrier
      Traps microorganisms, particles
      Neutralize bacteria via soluble proteins, secretory IgA

      Components:
      97% water, 3% solid--mostly Mucin (visicoelastic)
    • What are the bacteriostatic functions of mucus?

      How is it achieved in the main airways and alveoli?
    • Bacteriostatic = inhibit proliferation

      Do so via binding iron and limiting iron access of microbe

      In Main airways: lactoferrin does this
      In alveoli: transferrin does this
    • How can mucus directly kill microbes?
    • Lysozymes (hydrolyze cell walls of most bacteria, some fungi; inhibits chemotaxis, dec'd PMN free radical production)

      Defensins:
      Permeabilize bacteria--imbed into microbe cell membrane and form pore allow efflux of ions/nutrients
    • How does mucus augment immune clearance?
    • Opsonization!

      1) Collectins: mannose-BP, surfactant protein A bind and label bacteria for elimination

      2) Ficolins: opsonize/activate complement

      3) Complement: permeabilize bacteria
    • Why must the production of mucus be tightly regulated?
    • Too much mucus-->infection, cystic fibrosis/asthma/COPD

      Too little mucus-->inhalation injury, infection
    • What are the 2 layers of mucus and how do they differ?
    • Sol layer (bottom layer): aqueous, cilia move freely within; essential to ciliary function

      Gel layer: top layer, viscous, traps particles, transported cephalad by beating cilia
    • Describe the 9+2 structure of cilia.

      What does dynein do?
    • Central core has 2 MTs
      Outer ring has 9 doublets; connected to central core by radial spokes

      Inner and outer dynein arms = molecular motor
    • What is primary ciliary dyskinesia?

      Clinical effects?
    • Rare genetic disorder; impaired MCC (immotile cilia)

      Results in recurrent resp infections-->bronchiectasis; infertility (sperm), embryonic abnlts of asymmetry
    • Kartagener's Syndrome:
      Triad
    • Bronchiectasis
      Chronic Sinusitis
      Sinus inversus (uncommon)--abnl mvmt of embryonic epithelial tissue
    • Causes of acquired impaired MCC.
    • 1) viral infections-->epithelial damage, loss of ciliated epithelium
      2) cigarettes-->epithelial damage-->chronic bronchitis
      3) Bronchiectasis: mucostasis, chronic infectino
    • Why might pneumonia occur more with age?
    • Poly fn decreases with age (dec'd chemotaxis)
      Dec'd humoral immunity (dec'd T helper cells)
      Dec'd MCC
    • How does Cystic Fibrosis result in impaired MCC?

      Respiratory effects of this?
    • Mutation in CFTReceptors-->dysfn in epithelial cells in most organs (lung, panc, GU tract, sweat glands)

      Lose Cl- secretion and thus gradient that pushes water out of cells and into sol layer of mucus. Leads to inc'd mucus viscosity. Poorly cleared.

      Results in staph, pseudomonas, aspergillus infection; injury/inflammn (cyclic)-->respiratory failure
    • How does bronchiectasis appear on CT scan?
    • Abnormal thickened bronchi with abnormal tapering (don't taper)
    • CF complications in adults and infants.
    • Adults/adolescents: pansinusitis, hemoptysis, male infertility (absence of vas deferens)

      Infancy: meconium ilieus (thickened meconium in ileum)
    • Cystic Fibrosis:
      Treatment
    • Panc enzyme replacement
      IV and inhaled Abx
      Bronchodilators
      Nutritional support
      Need to HYDRATE and THIN mucus (inhaled hypertonic saline and inhaled DNase)

      Lung transplant
    • What is the effect of cough on airways and mucus?
    • Cough narrows airways, loosens mucus, removes it from airways
    • What are the 3 phases of cough? What occurs in each?
    • 1) Inspiratory Phase: Diaphragm fires
      2) Compressive Phase: forms subglottic pressure (against closed glottus), pressure quickly increases
      3) Expiratory phase: pressure opens glottis and drops
    • __________ weakness will exhibit adequate cough.
    • Patients with inspiratory weakness will still have ability to cough
    • Causes of expiratory weakness
      Effect on cough
    • Lower cervical injury (form of neuromuscular weakness)

      Can't produce pressure needed to cough and can't clear mucus
    • Cough effectiveness is proportional to mucus ______.
    • Depth
    • Cough effectiveness is inversely proportional to mucus ________.
    • Viscosity and elasticity
    • Alveolar macrophages:
      Role
    • -Ingest foreign particles in alveoli
      -Clear surfactant in alveolus
      -Exhibit pattern recognition receptors for LPS, DNA, RSV, etc.
    • Pulmonary Alveolar Proteinosis:
      What is it?
      Pathogenesis
      Effects
    • Alveoli fill with surfactant and protein due to dysfnl macs; results in hypoxia and dyspnea

      Fail to metabolize surfactant! protein also builds up

      Auto-Ab's against GM-Colony Stimulating Factor (req'd for mac dx/dy and fn)

      Predisposed to atypical infections (nocardia, fungi, other organisms)
    • What is acute respiratory distress syndrome?
    • Excessive inflammatory cellular response in lung
    • Collectins:
      What are they?
      Role
      Examples
    • Collectins are Surfactant Proteins A and D-->binds SIRP-alpha (signal inhibitory regulatory protein), which inhibits NFK-B release due to activated TLRs (which are bound to bacterial PAMP)

      Decreases mac phag and decreases inflamm response
    • Dendritic Cell:
      Role in Lung
      Location in lung
      How is it activated?
      Effects of activation?
    • Key APC in lung
      Resides in submucosa

      Activation via PRR-->mobilize/migrate to LN and activate naive T cells via presenting antigen
    • Which lymph nodes and lymphoid tissues are critical to presentation of antigens in the lung?

      Relevant immunoglobulins.
    • LNs: intraparenchymal, hilar, mediastinal LNs

      Bronchus-assocd lymphoid tissue (BALT) located at airway bifurcations (IgA production)
    • ________ cell is an important intermediary for neutrophil recruitment.
    • Epithelial cells!
    • Are neutrophils normally present in the lung?

      What's their function in the lung?
    • No, must be recruited (by epithelial cells detecting breach by pathogen)

      Nphil Role:
      1) Phagocytosis and subsequent generation of ROS
      2) Degranulation of antimicrobial proteins--lactoferrin and bacteriocidal permeability protein
    • What is a neutrophil extracellular trap?
    • NET: nphils release chromatin meshwork embedded with antimicrobial proteins, which have opsonic functions, bacteriocidal fns, and bacteriostatic fns
    • Are neutrophils part of adaptive or innate immunity?
    • Both!

      Innate because can phagocytose pathogens

      Adaptive bc can secrete cytokines to recruit T/B cells
    • Common cause of neutropenia.
    • Chemotx
    • Chronic Granulomatous Disease of the Phagosome:
      Cause/Mechanism
      Effects (general and on lung)
    • -Genetic

      -Defects in NADPH oxidase-->failure to produce Superoxide anion (ROS)-->recurrent infection and granuloma formation

      Results in LUNG BRONCHIECTASIS and FIBROSIS

      Diagnose via direct PMN NADPH oxidase testing
    • What patients are susceptible to pneumocystitis pneumonia?
    • Those with dysfn of adaptive immunity (HIV and AIDS)

      CD4 count dictates risk of secondary infections
    • What is the most abundant immunoglobulin in mucosal secretions?

      Result of its deficiency?
    • IgA

      IgA deficiency often asyx; sinus, lung, and GI infections. Rarely autoimmune disorders.

      Tx = IgA replacement
    • What is common variable immunodeficiency? Effects?
    • Deficiency of two or more Ig subclasses (A, G, M)

      ASsocd w/recurrent sinopulmonary infection, bronchiectasis, autoimmune disorders (GI disease, chronic lung dz, heightened susceptibility to lymphoma)