2nd Exam: Lung Disease 1 Flashcards
partial or complete collapse of the lung:
atela
fulmninant:
severe and sudden in onset.
Normal bronchus is lined by;
ciliated epi, cartilage for support
These divide alveoli:
septae containing many caps
prototype of immune-mediated d.:
asthma
asthma is one of __ types of immune response:
4
asthma:
long lasting, begins 1st-2nd decade, 1-2h episodes, stress, inhaled irritants, cold air, exertion, bronchial tube mm. tighten, thicken, inflamed walls, mucus filled airways
Pathogenesis of asthma:
type 1 hypersensitivity, exposure to antigen, it binds IgE, this activates inflammatory cells, mediators are released that cause the symptoms and inflammation
mediators released in asthma attack:
PG, leukotrienes, histamine, bradykinin
Types of inhaled irritants:
microbes, allergens, pollutants, oxidants, irritants
inhaled irritants that attract and activate macs, PMNs, and eosinophils:
CCL2, 5, 11, Il-6, 8, TNF-a, GM-CSF
Pwy antigen presentation to naive T-cell:
activate Th17 OR Th2 (routes) 1: eosinophil, cytokines, chemokines, cytotoxic products, lipid mediators 2. B cell w IgE, Mast cells and/or basophils, histamine, leukotrienes, PGD2, cytokines
IL required for Th2 cells to activate eosinophiis;
IL-5
IL’s required for Th2 cells to activate B cells
IL-4, 13
Eosinophils activate:
cytokines, chemokines, cytotoxic products, lipid mediators
mast cells and/ or basophils activate:
Leukotrienes, PGD2, cytokines
TF? Airflow is only restricted TO the lungs in asthma.
F. Both to and from
Asthma pathology:
vasod, mucus plus, desquamation of epi, mucus gland hyperplasia, sm hypertrophy and hyperplasia, thickened BM and sm, edematous submucosa w infiltration of granulocytes, infiltration of bronchi and para bronchial tissues w monocytes and lymhpos, thick mucus, inflammation
Prominent cell in response to asthma:
eosinophil
What do the eosinophils that respond to asthma secrete:
major basic protein, damaging
Diagnostic marker of asthma:
Charcot-Leyden crystals (eosinophil proteins)
What are Charcot-Leyden crystals?
eosinophilic proteins
Emphysema is aka:
COPD, centrilobular emphysema
Emphysema
common, chronic, progressive, mainly smokers, over 60 it gets severe, dyspnea, shortness of breath, cyanosis, disability, lungs hyperinflated, dilated air spaces in form of cysts/ blebs
Causes of tissue damage in emphysema:
ROS, inc mac elastase and metalloproteinases
These lead to ROS formation:
neutrophils, tobacco
Transport ROS to the blood stream:
IL-8, LTB4, TNF (8 Before tnf)
Role of neutrophils in emphysema:
create ROS, inc neutrophil elastase
These can increase neutrophil elastase:
neutrophils, congenital a1AT deficiency
3 roles of ROS in emphysema:
tissue damage, inactivation of antiproteases (essentially activating protease) (“functional: a1AT deficiency”, go to blood stream
Alveolar Type II cell:
septal cell, make surfactant
Alveolar Type I cell:
form wall
Some sm cells of the alveolar septum
knob cells
What happens with COPD?
septae destroyed, airspaces enlarged, O2 exchange reduced, fewer caps, loss of elasticity, can’t contract normally
Differential Dx of post-op dyspnea:
pulmonary emboli, pneumonia, diffuse alveolar damage (DAD)
Lines the wall of pts w acute lung injury (DAD):
hyaline mem
Causes of DAD (ARDS)
shock, trauma, surgery, burns, sepsis, oxygen therapy, smoke from house fire, drugs, aspiration, uremia (kidney failure), viral infection, newborn (surfactant)
ARDS sf:
Acute respiratory distress syndrome
Premature:
less than 37 wks gestation or under 2500 grams
Babies are more likely to be born preterm if:
maternal illness (GU tract infection), uterine incompetence-cervix dilates, multiple pregnancies, placental problems, premature labor, lack of prenatal care
Consequences of preterm birth for baby:
Death, immature organs vulnerable to many complications esp in lungs (RDS/HMD)
Appearance of HMD lungs :
firm, airless, dark red
Are HMD or normal newborn lungs crepitant?
normal
Greater than 50% of newborns are born under __ wks.
28
When ratios of this are less than 2:1 in the amniotic fluid, the risk of RDS is greater:
Lecithin, sphingomyelin
A large increase in lecithin happens at this wk of gestation:
35th
Pathologic lung changes that result from RDS:
atelectasis and hyaline membranes
TF? synthesis, storage, and release of surfactant are all reduced in HMD:
T
Does alveolar surface tension increase or decrease w dec alveolar surfactant?
Decreases
increased alveolar surface tension leads to:
atelectasis
atelectasis can lead to:
uneven perfusion, hypoventilation
Both uneven perfusion, hypoventilation can lead to
hypoxemia, Co2 retention, acidosis
Factors that lead to reduced surfactant synthesis, storage and release:
hypoxemia, CO2 retention, acidosis
Acidosis leads to:
pulm vasoc and reduced surfactant synthesis, storage and release
Pulm vasoc leads to:
hypoperfusion
pulm hypoperfusion leads to:
epi/ endo damage, blood leaks into alveoli, fibirin and necrotic cells (hyaline mem)
What is hyaline mem?
fibrin and necrotic cells
This is prominent in HMD:
lecithin
When are alveoli mature?
greater than 2:1, L:S ratio
Ischemia in HMD babies leads to:
cap perm, plasma leaks into alveoli, hyaline membrane formation (fibrin, necrosis)
Pneumonia can be:
bacterial, fungal, viral
Lung abscesses are usually due to:
bacterial infection
Pulmonary defense mechs:
nasal filtration, mucociliary escalator, macs, BALT, IgA, anti-proteases, anti-oxidants
The mucociliary escalator is in:
tracheobronchial tree
Where are macs found in the lungs?
alveoli
Immunologic pulmonary defense mechs:
BALT, IgA
Biochemical defense mechs:
anti-protease, anti-oxidants
Sources of acute pneumonia:
CON: Community acquired, nosocomial, opportunistic
Main organisms that cause community acquired pneumonia:
S. pneumoniae, H. influenze, influenza virus
Main organisms that cause nosocomial pneumonia:
Staph areus, gram negatives
Main organisms that cause opportunistic pneumonia:
CHAPP: CMV, herpes, adenovirus pseudomonas, pneumocystis,
Pop more prone to contracting opportunistic pneumonia:
elderly, immunosuppressed
Tissue site for bacterial pneumonia infection:
distal lung parenchyma
Bacterial pneumonia:
purluent exudate and consolidation (solidification) of lung, fever, shaking chills, productive cough, dullness to percussion, rales, chest x-ray infiltrates
Pt w productive cough, think:
bacterial pneumonia
Pathogenesis of bacterial pneumonia:
loss or suppression of cough reflex (anesthesia, coma), injury to mucociliary apparatus, inc secretions, impaired phagocytic activity of alveolar macs, alcohol, smoking, immune suppresision, previous lung injury (COPD, viral pneumonia), old age, exposure to cold
Factors that lead to impaired phagocytic activity of alveolar macs:
alcohol, smoking
Previous lung injury that can cause bacterial pneumonia:
COPD, viral pneumonia
Airway routes for spread of bacterial infection:
inhaled aerosols (env or person to person), aspirated vomit
Sources of bacterial infection in lungs:
airway, hematogenous (infection at other site)
Stages of bacterial infection in lung:
acute, resolving, organizing
Char’s of the acute phase of bacterial infection in lung:
polys in alveoli
Char’s of resolving stage of bacterial infection in lung:
no polys, many macs, infiltrates are cleared, alveolar walls intact
Char’s of organizing stage of bacterial infection in lung:
granulation tissue, fibrosis (terminal bronchioles and alveoli)
Anatomic patterns of bacterial pneumonia:
bronchopneumonia, lobar pneumonia
bronchopneumonia:
polys in distal airways
Risks for acquiring aspiration pneumonia:
caries, pd, poor oh, debilitation, alcohol abuse, loss of consciousness, surgery, vomiting, reflux, diminished gag reflex, abnormal swallowing
apiration pneumonia results in:
chemical injury and bacteria
This type of aspiration pneumonia may lead to abscess formation:
necrotizing, fulminant
Aspiration is more common here:
R bronchus, larger, shorter, more vertical
These cells react to foreign material in aspiration pneumonia:
giant cells
cxr:
chest x-ray
Lung abscess, routes of infection:
aspiration, previous pneumonia, bacteremia, from another organ
