Week 2 Flashcards

1
Q

Defense Mechanisms:

  • Innate response in lungs: Relies on? Recruits? What suppresses adaptive immune response? Clear what?
  • What patrols the vascular epithelium?
  • Sequence of innate receptor signaling? (3)
  • Bridge between innate and adaptive response?
  • Innate receptor signaling leads to? (5)
  • Where does adaptive response occur?
A
  • PAMPS; phagocytes and inflammation; alveolar MACs; junk in the lungs
  • Monocytes
  • PAMP binds TLR; APC present it and incite inflamm. respinse; Adaptive response later occurs
  • TLR’s
  • Cytokine produced; PMN recruitment; microbial killing; DC maturation; monocyte recruitment
  • Lymph nodes
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2
Q

Obstructive Lung Disease:

  • Bronchiolitis? Which airways?
  • Brhonchiolectasis? Effects what? Due to?
  • Types of obstruction? (3) All increase what?
  • Obstructive effect on airways? Leads to?
  • 5 types of asthma?
  • Long term asthma treatments? (6) Short term? (3)
A
  • Inflamm of membranous bronchioles; peripheral airways
  • Abnormal dilation of proximal medium sized bronchi; chronic bacterial infection; destruction of elastic components of airway
  • Intrinsic airway narrowing, floppy airways, decreased airflow; increased resistance
  • allergy (atopic); exercise induced; environmental; non-atopic; cough variant
  • Inhaled glucocorticoids; long acting B2 agonists; LT modifiers; omalizumab (anti IgE); Cromolym sodium; Theophylline (PDE inhibitor)
  • B2 agonists; anticholinergics; oral gc steroids
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3
Q

Obstructive Lung Disease:

  • Types of obstructive lung disease? (5)
  • 4 classes of COPD and their FEV/FVC and FEV values?
  • 4 classes of asthma and day symptoms? Night symptoms?
  • 2 parts of COPD? FEV/FVC values? DLCO?
  • goals of COPD treatment? (5)
A
  • Asthma, emphysema, chronic bronchitis, bronciolectasis, bronchiolitis
  • Mild (FEV/FVC 80); Moderate (FEV/FVC 2/mo); moderate persistant (daily; >1/wk); severe persistant (continual; frequent)
  • Emphysema (low; low), chronic bronchititis (low; high)
  • Decrease smooth muscle tone; decrease inflamm; treat infections; quit smoking; supplement O2
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4
Q
  • Imaging:
    1. ) Chest X-Ray: Ad? (3) Dis? (2)
    2. ) Chest CT: Ad? (3) Dis? (3)
    3. ) MRI: Ad? Dis? (2)
    4. ) V-Q scan: Ad? (3) Dis?
    5. ) PET scan: Ad? Dis? (2)
A
  • Cheap, low radiation, portable; nonspecific, insensitive to early disease
  • Overlapping densities covered, sensitive to early disease, better diagnostics; radiation, expensive, high false +
  • Great for heart and vascular; not great for lung imaging, poor spatial resolution
  • Good eval of ventiation/perfusion, great for PE, low radiation; only good for vascular issues
  • Metabolic activity; expensive, radiation
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5
Q
  • Histology:
  • 5 compartments? (5)
  • Acute Bronchitis: Infection of? Primarily?
  • Chronic bronchitis: 3 characteristics?
  • Asthma effects what? 3 characteristics?
  • Bronchioles don’t contain?
  • Types of bronchiolitis? (4) All lead to?
  • Types of granulomatous bronchiolitis? Cause? Cells Present? (2)
A
  • Airways, airspaces, alveolar septa, vessels, nodules
  • Bronchi; neutrophils in airways
  • Chronic inflamm, squamus metaplasia, mucus gland hypertrophy
  • Large airways; thickened subbasal lamina, eisino inflamm, mucus hyper secretion
  • Cartilage
  • Chronic, follicular, constrictive, granulomatous
  • Air trapping
  • Necrotizing = necrotic material via mycobacteria and fungus; non-necrorizing = sarcoid/beryllium; histiocytes (macs), giant multinucleated cells
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6
Q
  • Histology:
  • Cause of acute pneumonia?
  • Other types of pneumonia? (3)
  • Cause of organizing pneumonia? Present how?
  • Diffuse alveolar damage: What forms? Septa? Present how?
  • Emphysema? Common finding? (2) Smoking vs. alpha 1 a trypsin? (2)
  • Other smoking related diseases? (2) Cell found?
A
  • Neutrophils in airspace
  • Aspiration, eisinophillic, organizing
  • Fibroblast pugs; relatively healthy
  • hyaline membranes (pink fibrin ribbons); thickened; very sick
  • Enlarged airspaces; recoil bodies/ blebs; Smoking = upper lobes, centrilobular; a1 = lower lobes, panlobular
  • Respiratory bronchiolitis, desquamitive intersitital pneumonia; black pigmented macrophages
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7
Q
  • Histology:
  • Capillaritis can lead to? Sign?
  • Pulm. alveolar proteinosis: Airspaces with?
  • UIP effects? Age? Infectious? Patchy? Genous? Foci? Looks like? Worse where? Treatment?
  • NSIP: Uniform? Foci? Honeycomb? Treatable? 3 types?
  • Hypersensitivity pneumonia: Response to? What is effected? Find what on histology? (2)
  • Types of emboli? (2) Causes?
A
  • Diffuse alveolar hemorrhage; blood containing macs
  • pink fluid/ macs
  • Septa; older; no; yes; hetero; fibro foci; honeycomb; lower lobes; none
  • Yes homogenous; none; no; yes; cellular (inflamm.), fibrotic (fibrosis), or mixed
  • Foreign antigens (birds, mold, hot tub); septa; airway chronic inflamm., non-necrotizing granulomas
  • Thromboembolytic; talc = polarized crystals on histology with multinuc. giant cells from IV drug use
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8
Q
  • Histology:
  • Pulm htx leads to? (2)
  • Common causes of vasculitis? (2) Effect?
  • Sarcoid/ Beryllium disease: Granulomas? Colloagen is? Distribution?
  • Pulm. langherans cell histio.: Type of scar?
  • Carcinoid: Salt and pepper around? Prognosis?
  • Small Cell carcinoma: Crushed? Stain + for?
  • Squamus cell carcinoma: Common? Common histology finding?
  • Adenocarcinoma forms?
  • Large cell: Appear? (2) Lack features of?
A
  • Muscular hypertrophy; plexiform lesions (airway slits)
  • Infection or autoimmune; alveolar hemorrhage
  • well-formed non- nec grans; concentric; lymphatic
  • Star (stellate) scar
  • NE cells; good
  • small with little cytoplasm; bad
  • most common; keratin pearls
  • Glands with lumen
  • Large and bizarre; typical cell features of other carcinomas
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9
Q
  • Restrictive Lung Disease:
  • Overall cause of disease? Ex? (3)
  • Can also be caused by? (5)
  • Interstitial PV slope? Vol? DLCO?
  • Chest wall disease effect on PFT’s?
  • PFT’s for mixed obstructive and restrictive? (2)
  • 4 types of interstital lung disease? 2 treatable one?
  • Key physical exam findings? (3)
    1. ) Interstitial pulm. fibrosis: Caused by? Treatment? Ground glass?
    2. ) NSIP: Prognosis? Treatment?
A
  • Increased stiffness: More CT, surface tension, fluid
  • Chest wall disease, bony thorax, pleura, resp. muscles, soft tissues
  • Slope reduced, low, low
  • PV slope is the same; rest is low
  • Decreased volume and FEV/FVC
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10
Q

Restrictive Lung Disease:

  1. ) Respiratory Bronchiolitis: Progress to end stage fibrosis? Related to? Treatment? Don’t treat with? Looks like?
  2. ) Desquamative Inter. Pneu: Related to? Treat with? Location?
  3. ) Acute Inter. Pneu: Histologically called? Treatment? Symptoms? Alveoli?
  4. ) Organizing pneumonia: Called? Histological findings? Airways?
  5. ) Acute eisino. pneu: Presents like? DAD with? Treat?
A
  1. ) No; smoking; stop smoking; glucocorticoids; patchy ground glass
  2. ) Smoking; corticosteroids; distal airspaces
  3. ) Diffuse alveolar damage; none; flu-like; flooded with fluid
  4. ) BOOP; uniform granulation in distal airspaces; often neutrophillic alveolar infiltrates
  5. ) ARDS; esinophils; steroids
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11
Q
  • Pathophysiology of sleep apnea? Leads to? (2) Good treatment?
  • Most obstructive position?
  • Pressure relationships with collapse?
  • Best diagnostic tool?
  • Most likely definitively sucessful treatment?
A
  • Pharyngeal occlusion; hypoxemia and hypercapnia; Continous Positive Airway Pressure
  • Supine; REM sleep
  • Pcrit>Pds>Pus
  • Overnight polysomnography
  • Tracheostomy
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12
Q
  • Pneumonia:
  • Community acquired acute? (3) Atypical? (2)
  • Hospital acquired?
  • Aspiration?
  • Immunocompromised?
A
  • Strep pneu, hameopholis flu, staph aeureus; mycoplasma, chlamydia
  • gram - rods, staph aeureus
  • Anaeorobic
  • CMV
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