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183 Cards in this Set

  • Front
  • Back
Pulmonary Emobolism
Substance that lodges in branch of pulmonary and obstructs flow

lungs funtioning but hypoxic
#1 cause of Pulmonary Embolism
Clot from DVT, usally from calf area of immobolized person. Lodges in lungs
Predisposing factors to PE
Venous stasis (slugish circulation usually from bedress)

Hypercoagulability disorders

Damage to vein wall (usually trauma) platllets gather
Patho of PE
Thrombi disloged & floats free becoming an emboli

Most often lodges in lower lobes of lungs

Can obstruct 25% of pulmonary vessels w/out S/S (if more than 50% are obstructed - dangerous)

Pressure in pulmonary artery rises and can cause Rt sided heart failure
S/S of PE
Reslessness (caused by hypoxia)
apprehension
anxiety
sudden dyspena
tachycardia
tachypnea
sudden crushing substernal (with large emboli)
Px PE Treat/prevent clots in leg w/
range of motion/ambulation
do homans assessment
heparin SQ
Treatment PE
Emergency!! O2 Stat
heparin IV
Thrombolytic drugs
embolectomy
Thrombolytic drug
Streptokinase or t-PA

breaks clogs
Leading cause of CANCER death in men & women
Lung
Risk for lung cancer
SMOKING
Asbestos
coal dust
chemicals
Types of lung cancer
Squamous cell carcinoma
Adenocarcinoma
Large cell carcinoma
Small cell carcinoma
Lung Cancer that doubles in size in 100 days
Squamous cell
Large cell
Lung CA that doubles in size in 180 days
Adenocarcinoma
Lung CA that doubles in 33 days
Small cell carcinoma
Lung CA located in central lung
Squamous
small cell
lung cancer located in peripheral lung
adenocarcinoma
large cell
Lung cancer related to smoking
squamous cell (definitely)
large cell (definitely)
Small cell (strongest association with smoking)
20-35% of lung CA
Squamous Cell
35-40% of lung cancer
adenocarcinoma
5-20% lung cancers
large cell
15-20% of lung cancers
small cell
Treatment options for lung cancer
Squamous - surgery
Adenocarcinoma - surgery/chemo
Large cell - poor treatment options
Small cell - very poor (chemo) hardest to treat
lung cancer usually metastasizes to/near lymph nodes
squamous cell
lung cancer usually metastasizes to/near unpredictable locations far from lungs
adenocarcinoma
lung cancer usually metastasizes to/near distant locations quickly
large cell
lung cancer usually metastasizes - wide spread
small cell
squamous cell metastasize to
near by lymph
adenocarcinoma metastasize
unpredictable locations far from lungs
large cell metastasize
distant locations quickly
small call metastasize
wide spread metastis
Overall lung cancer S/S
Gradually chronic cough
SOB
wheezing
hemoptysis
dull chest pain
non-specific wt. loss and wasting
hemoptysis
coughing of blood
Chronic Obstructive Pulmonary Disease COPD
group of disease characterized by obstruction & difficult expiration

chronic & recurrent

Often associated w/ smoking, air pollution, occupational exposure
Name COPD's
Asthma
Status Asthmaticus
Chronic Bronchitis
Emphysema
Asthma effect how many people
15-17 million in US
most common chronic disease of children less then 17, but dx at any age
asthma
Asthma is characterized by
Reversible airway obstruction (bronchospasm & bronchoconstriction)

Airway inflammation

Hyper-responsiveness to stimuli (allergen, cold, exercise)
Types of asthma
Extrinsic (childhood onset)
Intrinsic (adult onset)
asthma childhood onset
extrinsic
asthma adult onset
intrinsic
extrinsic asthma associated w/
hayfever
family history
allergies
intrinsic asthma associated w/
respiratory infections
exercise
stress
asthma not associated w/ allergy
intrinsic
Other types/terms for asthma
exercise induced
occupational/environmental
drug
Patho of extrinsic asthma
allergen/irritant inhled
> mast cells attracted
>release of histamine

decrease in cilia actions causes inflammation of lining
hyperresponsiveness (broncospasm & bronchoconstriction)
increased vascular permeability > edema & thick mucus productions
S/S of asthma
wheezing
tightness in chest
Dsypnea
cough & sputum production

all that leads to anxiety/apprehension causing tachycardia,

sitting up to use accessory muscles to breath
Treatment for asthma
avoid allergens
peak flow meter for home
relaxation controlled breathing
sympathomimetics- epinephrine, alupent, isoprel (stimulates FFF)
bronchodilators (theophyline, relaxes smooth muscle)
corticosteriods - prednisone decreases inflammations
prednisone
corticosteriod that decreases inflammations
satus asthamaticus
servere bronchospasm that doesn't respond to usual treatment

need
epinephrine
o2
possible ventilator
Chronic Bronchitis
Inflammation of the bronchi due to chronic irritation from inhaled substances or infection lasting more than 3m/yr for 2+ years > chronic irreversible obstruction
Chronic obstruction
Chronic Bronchitis
Emphysema
Irreversible destruction of alveolar wall & abnormal enlargment of air sacs

loss of elasticity
loss of gas exchange surface area
loss of elasticity
loss of gas exchange
emphysema
Irritants cause chronic inflammation & swelling > scarring & fibrosis
chronic bronchitis
Inreased thick mucus production & increase the size of mucus producing glands
chronic bronchitis
cilia action decreased
chronic bronchitis
decreased mucus clearance because
decreased cilia action
obstruction of airlow due to mucus > hypoventilation & hypoxemia
chonic bronchitis
obstruction of airflow due to mucus can lead to
hypoventilation
hypoxemia
hypoxemia
deficient blood oxygen as measured by low arterial o2 & low hemoglobin saturation as measured by arterial blood gases or pulse oz
ventilation/perfusion mismatch (blood flow is ok (perfusion), but ventilation is obstructed)
chronic bronchitis
elastin is broken down in alveolar septum
emphysema
large air spaces r created
emphysema
airways collapse and trap air in distal alveoli
emphysema
can get air in, but expiration becomes difficult > hyperinflation
emphysema
air sacs stay full
hyperinflation
inflammation and hyperactivity > bronchospasm & narrowing of airways
emphysema
No mucus production
emphysema
no ventilation/perfusion mismatch
emphysema
can get air in but can't get air out
emphysema
ventilaton okay perfusion not
pulmonary embolism
ventilation/perfusion mismatch
ok vent/ perf not
pulmonary embolism
may be air pollution but 20x greater chance if u smoke
chronic bronchitis
may be inherited or due to smoking
emphysema
over wt.
30-40's
history of smoking
SOB
wheezing
exercise intolerance
increased sputum in am
chronic cough
prolonged expiration
chronic bronchitis
thin
in 50's
SOB for 3-4yrs
history of smoking
emphysema
s/s breathing of chronic bronchitis
SOB
wheezing
exercise intolerance
increased sputum in am
chronic cough
prolonged expiration
dyspnea on exertion
no wheezing
prolonged labored expiration
emphysema
a disease that takes some work to breathe
chronic bronchitis
extreme work to breathe
emphysema
blue (hypoxia) bloater (fluid/mucus)
chronic bronchitis
pink puffer
emphysema
often must lean foward to breath
pursed lip breathing
emphysema
productive cough w/ copious sputum
chronic bronchitis
hyperactivity of mucus cells
chronic bronchitis
minimal to no cough & mucus
emphysema
barrel chest
emphysema
cyanosis in end-stage
chronic bronchitis
gurgles & rhonci
chronic bronchitis
decreased breath sounds
distant & soft sounds
no fluid in lungs
emphysema
Increased Co2 decreased o2
chronic bronchitis
hypercapnia & hypoxia
chronic bronchitis
hypoxia
decrease in tissue o2
hypercapnia
greater than normal amounts of carbon dioxide in blood
T or F chronic bronchitis is respiratory acidosis
T
relatively normal blood gases
emphysema
death of chronic bronchitis pt
early age
death of emphysema pt
older age
Chronic Bronchitic treatment
limit o2
avoid smoking & irritants
control respiratory infections
good nutrition & fluids
breathing training
bronchodilators
percussion & postural drainage
emphysema treatment
limit o2
avoid smoking & irritants
control respiratory infections
good nutrition & fluids
breathing training
meds for chronic bronchitis
bronchodilators (theophyline)
expectorants
corticosteriods
adrenergics
Limit o2 for chronic bronchitis and emphysema pt because
if given to high a concentration will decrease stimulus to breath
how much o2 for chronic bronch. & emphysema pt
no more than 2L
atelectasis
collapse of lung tissue (alveolar)
several diseases cause _______ = collapse of lung tissue
atelectasis
Diseases caused by atelectasis
ARDS
Infant RDS
Respiratory failure characterized by acute lung inflammation and alveolar damage
hypoxia that doesn't responds to o2 treatment
ARDs
ARDS stands for
adult respiratory distress syndrom
Complications not really a disease
ARDS
ARDS is
Respiratory failure
acute lung inflammation
alveolar/capillary membrane damage > hypoxia that doesn't respond to o2 treatment
causes of ARDS
sepsis
major trauma
shock
surgery
burns
pneumonia
patho

Injury to alveolar capillary membrane increases cap permeability leading to fluid in alveoli

surfactant becomes damaged & alveoli collapse & become hard to inflate again

Increased respiration & impaired gas exchange

fibrosis & decreased pulmonary compliance (hyaline membrane form)

leads to resp. failure & MODS
ARDS
hyaline membrane
a fibrous covering of the alveolar membrans in infants caused by lack of surfactant
S/S of ARDS
follows an event

low blood volume state like shock
sudden resp. distress > tachycardia, dyspnea, low o2
hypoxia unresponsive to o2
treat the cause
humidified o2 & PEEP
incubation w/ ventilator if needed
ARDS
PEEP
positive end-expiratory pressure that forces o2 in
leading cause of death in premature babies
infant respiratory distress syndrome
Infant RDS is associated w/
pulmonary immaturity less than 30 weeks (lack of surfactant)
infantRDS patho
increase pressure is needed to inflate alveoli > atelectasis

alveoli collapse between each breath or baby can't work hard enough to open it all
alveoli collapse between each breath or can't work hard enough to open it all
infant RDS
infant RDS S/S
tachypnea
shallow respiration
retractions
working hard to breathe
decreased breath sounds
low o2 saturation
central cyanosis (due to hypoxia)
Monitor o2
o2 by PEEP
mechanical ventilation
surfactant replacement/therapy
treatment for Infant RDS
pneumothorax
collapsed lung not just alveoli because

air gets between the linings of the pleura & lung collapse
destroys the negative pressure of the respiratory system
pneumothorax
names of pneumothorax
primary
secondary
open
tension
primary pneumothorax
occurs spontaneously in health people
usually smokers age 20-40
rupture of air blebs in top of lungs
secondary pneumothorax
due to existing pulmonary diseas
open pneumothorax
fracure ribs & medical procedures "puncture lung"
tension pneumothorax
air gets in (due to trauma) but can't get out again increased pressure in chest (like a one-way valve)
S/S pneumothorax
sudden chest pain
increased respiration (1 lung)
increased heart rate (1/2 o2)
chest asymmetry
mediastinal shift to ok side
decreased breath sounds or absent on one side
Dx CXR and o2 sat & chest auscultation
pneumothorax
Treatment - Sometime spontaneously resolves (whole lung may not be collapsed)
chest tube to reinflate lung
pneumothorax
TB caused by
mycobacterium TB
Increased in blacks, hispanics, homeless, refugess & HIV
TB
an acid-fast bacilli
TB
TB transmitted
airborne - droplet nuclei, from secretions in small droplets lodges in the upper lobes of the lung
Lung destruction is NOT due to the organism but the immune response to the organism
TB
TB test shows
if you have been sensitized to the organism - may not actually be in the lungs anymore
Primary TB infection patho
exposure usually unknown (breathe in TB directly to alveoli (so small))
macrophages engulf the bacillus & WBC fuse around bacillus to isolate it
encapsulation occurs (ghons tubercle) & central portion of tubercle necroses
scar tissue forms around the tubercle
+ TB test can be seen on chest xray
remains dormant until tuberucle is broken down during times of immunosupression
encapsulation (primary TB)
ghons tubercle
caseous necrosis
central portion of tubercle necroses
Usually DONT get active TB disease with
intial infection; get it from secondary infection
Secondary TB (reactivation)
reactivation of healed tubercle during times of deceased defenses
Low grade fever
night sweats
fatigue
wt. loss
decreased appetite
eventual cough w/ mucoid
bloody sputum eventually
secondary TB
+ TB test
sputum culture
CXR
secondary TB
Gold standard for TB test
sputum culture
Meds for secondary TB
INH
rifampin
ethambutol
Multiple drugs for a long time to treat
secondary TB
Drugs usally give 2+ at a time many people exp hiv pt get a drug resistant form

course of treatment 6-9m
hiv pt will take meds longer
secondary TB
viral infection of the larynx
croup
inflammatory edema of the --------- caused by H. flu virus
epiglottitis
viral infection of the lower airway often infected with RSV
bronchiolitis
RSV
respiratory syncytial virus
childhood respiratory diseases
croup
epiglottitis
bronchiolitis
inflammation of the vocal cords down
croup
bronchioles swell and cellular debris forms little plugs > can get air in but not out
bronchiolitis
child resp. disease

children 3m to 2yrs; more common in winter
croup
child resp. disease

children 2-4yrs
epiglottitis
child resp. disease

family with cold transmitis it to a child less then 2yrs old
bronchiolitis
S/S croup
barking cough
inspiratory stridor
crying
anxiety
preceded by URI
S/S epiglottitis
VERY soar throat
sudden airway obstruction
can't swallow
drooling
pale
anxious
fever
S/S bronchiolitis
Wheezing
dyspnea
crackles
retraction
sputum
tachypnea
fever
listessness
cool mist/ mist tent or runn shower
cool vaporizer
night air
o2
hydration
epinephrine
treatment of coup
ER quickly (trach & antibotics)
don't lay child down
don't look down throat
epiglottitis
o2 - humidified
bronchodilators
prevent dehydration
bronchiolitis
heridity autosomal recessive disorder of exocrine glands
cystic fibrosis
exocrine glands in lungs, on skin, & in pancreas
cystic fibrosis
Cystic fibrosis patho
gene mutation leads to thick mucus & stasis of mucus (anywhere mucus cells are located)
thick tenacious sputum - can't cough up
recurrent pulmonary disorders
dyspnea
tachypnea
retractions
crackles/gurgles > chronic lung disease
pancreatic insufficiency > malabsorption of food
S/S of cystic fibrosis
Dx for Cystic Fibrosis
sweat test - stimulate skin with electrode & pilocarpine

"salty baby"

usually dx at 6m of age
Tx for Cystic Fibrosis
Respiratory support - because respiratory problems kill them
chest visotherapy (postural drainage & percussion)
expectorants
treat infection quickly
pancreatic enzymes
used to be rare to live past 20, now many live beyond 30 and have children
cystic fibrosis
Pneumonia
acute inflammation of the alveoli & bronchi

may be bacterial or viral
pneumonia organism - community
strep. pneumoniae
Nosocomial
E. Coli
Klebsiella
Pseudamonas
staph. Aureus
Can be lobar or bronchial
pneumonia
aspirations of organism spread by aerosol (cough or contaminated air)
Inflammatory response - accumulation of exudate, RBC & bacteria in alveoli
consolidation of lobe as exudate fills air spaces & thickens (can't be coughed up)
Patho bacterial pneumonia
viral pneumonia doesn't cause
exudate
sudden onset of malaise
shaking chills
Increased WBC
Fever
cough
crackles
pleuritic pain
sputum color varies
S/S of bacterial pneumonia
destroys cilited epithelial cells leading to increase mucus production with poor clearance
bacterial pneumonia
slow onset
low fever
cough
crackles
S/S of viral pneumonia
mild to self-limiting disease

can have secondary infection with bacteria
viarl pneumonia
Dx pneumonia
find the organism
Tx pneumonia
antibotics (bacterial)
deep breathing & coughing exercises
hydration