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
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
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
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
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
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
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
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
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
10
Q
Restrictive Lung Disease:
- ) Respiratory Bronchiolitis: Progress to end stage fibrosis? Related to? Treatment? Don’t treat with? Looks like?
- ) Desquamative Inter. Pneu: Related to? Treat with? Location?
- ) Acute Inter. Pneu: Histologically called? Treatment? Symptoms? Alveoli?
- ) Organizing pneumonia: Called? Histological findings? Airways?
- ) Acute eisino. pneu: Presents like? DAD with? Treat?
A
- ) No; smoking; stop smoking; glucocorticoids; patchy ground glass
- ) Smoking; corticosteroids; distal airspaces
- ) Diffuse alveolar damage; none; flu-like; flooded with fluid
- ) BOOP; uniform granulation in distal airspaces; often neutrophillic alveolar infiltrates
- ) ARDS; esinophils; steroids
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
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