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33 Cards in this Set

  • Front
  • Back
general pathology (5)
inhalation of the offending agent
macrophages engulf and transport particles and then expel these particles into the mucus
particles eventually accumulate in the alveoli (may trigger further immune response)
fibroblasts secrete reticulin to entrab macrophages
pulmonary interstitial fibrosis ensues
features of siliconiosis (3)
most common pneumoconionis in the world
occurs in mining, drilling, sandblasting
intense fibrotic reaction with silicon dioxide
what infection does siliconiosis most predispose for
mycobacterial (TB)
symptoms of siliconiosis
OSOB with exercise
occasional bluish skin at ear lobes or lips
loss of appetite
3 stages of siliconiosis
acute - 5 years (widespread consolidations with CXR)
accelerated - 5-10 years
chronic - 10+ years
two types of chronic disease
simple or progressive massive fibrosis
treatment of siliconiosis (2)
mostly supportive (O2, rehab)
should have yearly TB skin tests
prognosis of siliconiosis (2)
acute can be rapidly fatal
progressive massive fibrosis has a more varried course and may lead to progressive impairment and resp failure
keys in asbestosiosis (4)
fibrosis of the lung parenchyma due to asbestos exposure
asbestos is used for insulation, reinforcing matertials, etc
seen in plumbers, custodians, and maintenance workers
in advanced cases, lungs are stiff and small
symptoms of asbestiosis (2)
similar to chronic bronchitis
increased sputum
manifestations of asbestiosis (5)
very slow manifestation (20-40 years)
pulmonary fibrosis
lung cancer
laryngeal cancer
GI cancers
asbestiosis dx (2)
pleural plaque and linear opacities in CXR
asbestos in histologic exam
treatment for asbestiosis (5)
no effective treatment
supportive care
stop exposures
vaccination against influenza and pneumococci
lung transplantation in selected cases
black lung symptoms (4)
no pathognomic symtoms - hx is key
chronic cough
sputum prduction
nodular opacities in CXR
manifestation of simple black lung
often asymptomatic
manifestations of progressive massive fibrotic black lung
progressive dyspnea
pulmonary HTN
respiratory failure
diagnosis of black lung
coal macules in histologic exam (pin head sized collections of macrophages filled with black coal)
onset of beryllium disease
show gradual onset
acute beryllium disease
intense inflammatory reaction resembling pneumocystis
chronic beryllium disease
granulomatous disease primarily affecting the lung
diagnosis of beryllium disease (4)
made by hx
histologic exam
lab confirmation through a lymphocyte transformation test
CXR may range from normal to diffuse interstitial infiltrates and hilar adenopathy
linear patterns in CXR
where are thermal injuries confined to?
upper respiratory
what can cause airway obstruction
laryngeal edema
complications of thermal injury (4)
immediate reaction --> direct injury
CO and cyandie poisoning
acute respiratory distress syndrome - 24-48 hours after thermal injury
late onset pulmonary complication
symptoms of thermal injuries (7)
symptoms of smoke inhalation (5)
hypoxemia may progressively worsen
pulmonary edema may develop
CXR may reveal diffuse, patchy infiltrates
infection often ensues due to compromised defenses
upper airway obstruction can occur
treatment for smoke inhalation (2)
close observation
100% O2
neuro symtoms of CO poisoning (3)
visual changes
breakdown of muscle fibers resulting in the release of muscle fiber contents (myoglobin) into the bloodstream. some of these are harmful to the kidney and frequently result in kidney damage
diagnosis of CO poisoning (2)
made by history
COHb level on ABG
high altitude cerebral edema
high altitude pulmonary edema (more common than HACE)
in drowning
metabolic acidosis