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558 Cards in this Set

  • Front
  • Back
conducting zone
nose, pharynx, trachea, bronchi, bronchioles, terminal bronchioles
cartilage is present where?
trachea and bronchi
where is anatomic dead space
conducting zone (nose to the terminal bronchioles)
where does gas exchange occur
respiratory zone
(resp bronchioles, alveolar ducts, alveoli)
pseudostratified columnar ciliated cells extends to
respiratory bronchioles
goblet cells extend to
terminal bronchioles
type 1 pneumocytes
97% of alveolar surfaces
line alveoli
squamous
thin for gas diffusion
type II pneumos
secrete surfactant (dec surface tension)
cuboidal and clustered
precursors to type I and 2
proliferate during lung damage
clara cells
non ciliated
columnar
secretory granules
secrete part of surfactant
degrade toxins
reserve cells
what indicates fetal lung maturity
lecithin to sphingomyelin ratio or > 2 in amniotic fluid
bronchopulmonary segment
center:
tertiary bronchus
2 arteries (bron and pulmonary)
borders:
veins and lymphatics
what runs in the center of bronchopulmonary segment
arteries and airways
(bronch and pulm artery, bronchus)
what runs along borders of bronchopulmonary segment
veins and lymphatics
pulmonary arteries carry
deoxygenated blood from right side of heart
what maintains pulmonary arterial pressure at relatively constant levels throughout cardiac cycle
elastic walls
right lung has how many lobes
3
left lung has how many lobes
2 (and then the lingula)
side of inhaled foreign bodies and why
right
right main stem bronchus is wider and more vertical
aspirate a peanut while upright
lower part of right inferior lobe
aspirate a peanut while supine
superior part of right inferior lobe
relation of pulmonary artery to bronchus at each lung hilus
RALS

right anterior
left superior
horizontal fissure
sep superior and middle lobes of right lung
oblique fissure
sep middle and inferior lobes or right lung

or sep superior and inferior or the left lung
what perforates diaphragm at T8
IVC
what perforates diaphragm at T10
Esophagus
vagus
what perforates diaphragm at T12
aortic hiatus (red)
thoracic duct (white)
azygous vein (blue)
diaphragm innervation
C3,4,5
pain from diaphragm is referred
to shoulder
muscles of inspiration, normal breathing
diaphragm
muscles of expiration, normal breathing
passive
muscles of inspiration, exercise
external intercostals
scalenes
sternomastoids
muscles of expiration, exercise
rectus abdominas
internal and ext obliques
transversus abdominis
internal intercostals
dipalmitoyl phosphatidylcholine (lecithin)
surfactant
what does surfactant do
dec alveolar surface tension
inc compliance
dec work of inspiration
deficient in neonatal RDS
surfactant
collapsing pressure
2(tension)/radius

surfactant decreases T as r decreases
lung products (5)
1. surfactant
2. PGs
3. histamine
4. angiotensin converting enzyme
5. kallikrein
kallikrein
activates bradykinin
ACE
angio 1 to angio 2
inactivates bradykinin
ACE inhibitors cause cough: mech
inhibit ACE, so
can't inactivate bradykinin, so
increased bradykinin means cough and angioedema
histamine does what
bronchoconstricts
lung has tendency to what on expiration as radius decreases
collapse
what prevents lung collapse on expiration as radius decreases
surfactant (2T/r)
residual volume (RV)
air in lung after maximal expiration
can't be measured on spirometry
expiratory reserve volume (ERV)
air that can still be breathed out after normal expiration

(your maximum expiration)
tidal volume (TV)
air that moves into lung with each quiet inspiration (500 ml)

(normal breath)
inspiratory reserve volume (IRV)
air in excess of tidal volume

maximum inspiration
vital capacity
everything but RV:

TV + IRV + ERV
(normal breath + max insp + max exp)
functional residual capacity
RV + ERV = 0 energy state
Residual vol + max exp

vol in lungs after normal expiration
0 energy state
functional residual capacity
FRC = RV + ERV
inspiratory capacity
IRV + TV
Total lung capacity
IRV + TV + ERV + RV
physiological dead space equation
Vd= Vt (PaCO2 -PeCO2)/PaCO2

Tidal vol(arterial - expired air PCO2)/arterial

anatomical dead space in airways + functional dead space in alveoli
largest contributor of functional dead space
apex of healthy lung
anatomical dead space of conducting airways + functional dead space in alveoli
physiological dead space
tendency for lungs and chest wall
lungs to collapse in
chest to expand out
at FRC, what is the lung/chest wall relationship
lung inward pull is balanced by chest wall outward pull

system pressure is atmospheric
at FRC, pleural pressure is
negative (lungs inward pull balances chest wall outward pull)
inc Cl-
right or left shift
R
inc H+
right or left shift
R
inc CO2
right or left shift
R
inc 2,3 BPG
right or left shift
R
inc temp
right or left shift
R
right shift means what
inc O2 unloading to tissues
fetal Hem shifts curve left- why?
lower affinity for 2,3 BPG
so higher O2 affinity
relaxed form of hemoglobin-
right or left
L
high affinity for O2
taut form of hemoglobin-
right or left
R
low affinity for O2
Most CO2 transported in blood is in what form
bicarb
CO2 transport form that is bound to hemoglobin
carbamate-
CO2 binds to amino acids in globin chain at N terminus (not bound to heme)
CO2 binding favors what form of hemoglobin
taut (right)
promotes O2 unloading
negative allosteric regulation
methemoglobin
oxidized form of hemoglobin (Fe 3+)
does not bind O2 as readily
inc affinity for CN-
methemoglobin causes
tissue hypoxia
from dec O2 sat and dec O2 content
carboxyhemoglobin causes
tissue hypoxia
from dec O2 sat and dec O2 content
due to dec O2 carrying cap (left shift)
so dec O2 unloading to tissues
carboxyhemoglobin
form of hemoglobin bound to CO in place of O2
CO vs O2 affinity for hemoglobin
CO has 200x greater affinity than O2 for hemoglobin
treat CN- poisoning
nitrites to oxidize hemoglobin to methemoglobin, which binds CN-

then use thiosulfate to bind the CN-, forms thiocyanate, renally excreted
tx methemoglobinemia
methylene blue
and vit C
shape of oxygen hemoglobin dissociation curve and why
sigmoidal
positive cooperativity
each binding has higher affinity for O2
right shift changes affinity how
decreases hem affinity for O2
inc pH
right or left shift
left (dec H+)
altitude
right or left shift
R
exercise
right or left shift
R
inc metabolic needs
right or left shift
R
inc P50
right or left shift
R
pulmonary circulation-
resistance is high or low
compliance is high or low
low resistance
high compliance
dec in PAO2 causes
hypoxic vasoconstriction that shifts blood away from poorly ventilated areas of lungs to well ventilated areas
perfusion limited gases
O2
CO2
N2O
O2
perfusion or diffusion limited
perfusion
CO2
perfusion or diffusion limited
perfusion
N2O
perfusion or diffusion limited
perfusion
perfusion limited means
crosses membrane easily, early eq

gas equilibrates early along the length of the capillary

must inc blood flow to inc diffusion
diffusion limited means
doesn't cross membrane easily, late eq

gas does not equilibrate by the time blood reaches the end of the capillary
diffusion limited gases
O2 in emphysema or fibrosis
CO
CO
perfusion or diffusion limited gas
diffusion
consequence of pulmonary hypertension
cor pulmonale-
right ventricular failure
(Jug venous distension, edema, HSM)
diffusion equation
Vgas = A/T x Dk(P1-P2)

A= area
T= thickness
Dk(P1-P2) = diff in partial pressures
Diffusion equation
emphysema- what variable changes?
A (area) decreases

Vgas = A/T x Dk(P1-P2)
diffusion equation
what variable changes with pulmonary fibrosis?
T (thickness) increases

Vgas = A/T x Dk(P1-P2)
normal pulmonary artery pressure is
10-14 mmHg
pulmonary htn pressure
greater than or equal to 25 mmHg or
greater than 35 mmHg w/exercise
pulmonary htn leads to
atherosclerosis
medial hypertrophy
intimal fibrosis of pulmonary arteries
primary pulmonary htn is due to
inactivating mutation in BMPR2 gene which normally inhibits vascular smooth muscle proliferation
secondary pulmonary htn is due to
COPD (destroys lung parenchyma)
mitral stenosis (inc resist->inc press)
recurrent thromboemboli
autoimmune (fibrosis, med hypert)
sleep apnea (hypoxia-> vasocon)
high altitude (vasoconstriction)
left to right shunt (inc sheer stress causes endothelial injury)
course of pulmonary htn
severe resp distress ->
cyanosis and RVH ->
death from decompensated cor pulmonale
pulmonary vascular resistance equation
PVR = Ppulm art - P Latrium/ C.O.

PLatrium is pulm cap wedge press
resistance
R = deltaP/Q

R = 8nl/pi r^4
n= viscosity, l = length, r = radius
change in pressure
delta P = QR

(remember- it goes in alphabetical order!)
arterial O2 content
(O2 binding cap x % sat) + dissolved O2

=1.37(Hgb)(%sat) +0.0031PaO2
1.37(Hgb)(%sat) +0.0031PaO2
oxygen content (CaO2)
8nl/(pi r^4)
= R
P/Q
=R
QR
=P
normal Hgb amount in blood
15g/dL
1 gram of Hgb binds how much O2
1.34 mL O2
cyanosis results when deoxygenated Hb is
> 5 g/dL
O2 content of arterial blood falls as
Hb falls
as Hb falls, what happens
O2 content falls
O2 sat is the same
PO2 is the same
arterial PO2 dec with chronic lung disease because
physiologic shunt decreases O2 extraction ratio
oxygen delivery to tissues =
C.O. x O2 content of blood =
C.O. x (CaO2 -CvO2)
alveolar gas equation
PAO2 = PIO2 - PACO2/R
PAO2 = (PB-PH2O)F1O2 -PACO2/R
=(760-47)0.21- PACO2/R
= 150- PACO2/ 0.8
PIO2
PO2 in inspired air
(PB-PH2O)F1O2
Respiratory quotient (R)
part of alveolar gas equation
= 0.8
=CO2 produced/O2 consumed
A-a gradient
PAO2-PaO2 = 10-15 mmHg
increased A-a gradient
hypoxemia due to:

shunt
V/Q mismatch
fibrosis (diffusion block)
hypoxemia with normal A-a gradient
high altitude
hypoventilation
hypoxemia definition
decreased PaO2
(arteriolar PO2)
hypoxia definition
decreased O2 delivery to tissues
causes of hypoxia
dec Cardiac Output
hypoxemia
anemia
cyanide poisoning
CO poisoning
ischemia definition
loss of blood flow
2 general causes of ischemia
impeded arterial flow
reduced venous drainage
V/Q normal values
normally V/Q = 1 for gas exchange
apex = 3 (wasted ventilation)
base = 0.6 (wasted perfusion)
where are V and Q the greatest?
base of the lung
zone 1 of the lung
PA > Pa > Pv
V/Q = 3
increased dead space (wasted ventilation)

high alveolar pressure compresses capillaries
zone 2 of the lung
Pa > PA > Pv

Q is increased
zone 3 of lung
Pa > Pv > PA
V/Q = 0.6
both V and Q are greater than at apex

recruitment and distention!!!
where is V greatest
base
where is Q greatest
base (it's greater than V)
where is V/Q greatest
apex
where is PO2 greastest
apex
where does TB live and why
apex
greatest PO2
exercise/inc cardiac output does what to apical capillaries
what is the result?
vasodilates them
result is a V/Q ratio that approaches 1
V/Q = 0
shunt (airway obstruction)
V is 0
100% O2 does not improve PO2
V/Q = infinity
dead space
blood flow obstruction
100% O2 improves PO2
no V
shunt
V/Q = 0
no Q
dead space
V/Q = infinity
shunt is what type of problem
no V
oxygen problem
dead space is what type of problem
no Q
CO2 problem
3 forms of CO2 transport
bicarb
carbamino (bd to hgb)
dissolved in blood
how does CO2 become bicarb?
carbonic anhydrase:
CO2 + H2O -> H+ +HCO3-
in lungs, what promotes dissociation of H+ from Hb and then what happens?
oxygenation of Hb promotes dissociation,
this shifts eq towards CO2 formation so CO2 is released from RBCs

(Haldane effect)
Haldane effect
oxygenation of Hb promotes dissociation of H+
this shifts eq towards CO2 formation so CO2 is released from RBCs
Bohr effect
in peripheral tissues, inc H+ shifts curve to right, unloading O2 and picking up CO2
high altitude does what to ventilation
acute and chronic inc
high altitude does what to erythropoietin
inc
(which inc hematocrit and hemoglobin)

this is chronic hypoxia
high altitude does what to 2,3 DPG
inc it

(it binds to Hb so Hb can release more O2)
high altitude does what to mitochondria
inc
high altitude does what renally
inc excretion of bicarb to compensate for metabolic alkalosis
high altitude does what to pulmonary vessels
chronic hypoxic vasoconstriction->
RVH
exercise does what to CO2 production
inc
exercise does what to O2 consumption
inc
exercise does what to ventilation rate VA
inc ventilation rate to meet O2 demand
exercise does what to V/Q ratio
it becomes more uniform from apex to base
exercise does what to pulmonary blood flow
inc it due to inc cardiac output
exercise does what to cardiac output
inc
exercise does what to pH
dec it with strenuous exerc, due to inc lactic acid
exercise does what to PaO2
nothing
exercise does what to PaCO2
nothing
exercise does what to venous CO2 content
inc
COPD
obstruction of air flow resulting in air trapping in the lungs,
airways close prematurely at high lung volumes
COPD:
airways close prematurely at high lung volumes, which results in
inc RV and dec FVC
COPD
PFTs
dec FEV1
dec FVC
dec FEV1/FVC ratio
V/Q mismatch
inc TLC
inc RV
chronic bronchitis
blue bloater
hypertrophy of mucous secreting glands in bronchioles,
disease of small airways

inc Reid index
Reid index
gland depth/thickness of bronchial wall

> 50% with chronic bronchitis
chronic bronchitis criteria
productive cough for > 3 consecutive months in > 2 yrs
chronic bronchitis symptoms
wheezing
crackles
cyanosis (early hypoxemia)
late onset dyspnea
emphysema
pink puffer
enlargement of air spaces
decreased recoil from destruction of alveolar walls
centriacinar emphysema is caused by
caused by smoking
panacinar emphysema is caused by
alpha 1 antitrypsin deficiency
liver cirrhosis
paraseptal emphysema is associated with
bullae that can rupture
spontaneous pneumothorax in young healthy males
centriacinar emphysema location
prox acinar
upper lobes
panacinar emphysema location
diffuse
lower lobes
paraseptal emphysema location
distal acinar
emphysema findings
dyspnea
dec breath sounds
tachycardia
late onset hypoxemia due to loss of capillary beds
early dyspnea
inc elastase activity
emphysema
inc elastase activity in emphysema causes what
inc lung compliance due to loss of elastic fibers
exhale through pursed lips- what and why?
emphysema
inc airway pressure and prevent airway collapse during exhalation
asthma
bronchial hyperresponsiveness causes reversible bronchoconstriction
asthma path features
smooth muscle hypertrophy
curshman spirals (shed epithelium from mucus plugs)
charcot ledyen crystals (eosinophils)
asthma triggers
viral URI
allergens
stress
asthma findings
cough
wheezing
dyspnea
tachypnea
hypoxemia
pulsus paradoxus
dec I/E ratio
mucus plugging
bronchiectasis
chronic necrotizing infection of bronchi
permanently dilated airways
bronchiectasis findings
purulent sputum
recurrent infections
hemoptysis
bronchiectasis is associated with
bronchial obstruction
CF
poor ciliary motility
Kartaganers
can dev aspergillosis
types of COPD
chronic bronchitis
emphysema
asthma
bronchiectasis
restrictive lung disease
restricted lung expansion
dec lung volumes
either poor breathing mechanics or interstitial lung disease
restrictive lung disease
PFTs
dec FVC
dec TLC
FEV1/FVC ratio > 80%
restrictive lung disease:
poor muscular effort
causes
polio
myasthenia gravis
restrictive lung disease:
poor structural apparatus
causes
scoliosis
morbid obesity
restrictive lung disease-
interstitial lung diseases
ARDS and neonatal hyaline memb.
pneumoconioses (coal minors)
sarcoid
idiopathic pulm fibrosis
goodpastures, wegners
eosinophilic/histiocytosis X
drugs
drugs causing IPF
bleomycin
busulfan
amiodarone
neonatal respiratory distress
surfactant def
inc surface tension
alveolar collapse
when is surfactant made during gestation
after 35th week
lecithin to sphingomyelin ratio in amniotic fluid is what in neonatal resp distress
< 1.5
risk of what with neonatal resp distress
persistantly low O2 tension-> inc risk of PDA
risk factors for neonatal resp distress
premature
maternal diabetes (high insulin)
cesarean
treat neonatal resp distress
maternal steroids before birth
artificial surfactant after birth
ARDS is caused by
trauma
sepsis/shock
gastric aspiration
uremia
acute panc
amnio fluid embolism
ARDS
diffuse alveolar damage -> inc alveolar capillary permeability -> protein rich leakage into alveoli->
formation of intra alveolar hyaline membrane
ARDS
initial damage is due to
neutrophils
toxic to the alveolar wall
this activates coag cascade or ROS
obstructive lung volumes are
greater than normal
restrictive lung volumes are
less than normal
FEV1/FVC ratio in obstructive and restrictive lung diseases
FEV1 and FVC are reduced in both but FEV1 is more reduced in obstructive,
sooo dec ratio with obstructive.
witches hat curve
(flow volume curve)
restrictive
higher volume, scooped out curve
(flow volume curve)
obstructive
sleep apnea
stops breathing for at least 10 sec repeatedly during sleep
central sleep apnea
no respiratory effort
obstructive sleep apnea
respiratory effort
sleep apnea associations
obesity
snoring
pulm htn
arrhythymias
tx sleep apnea
wt loss
CPAP
surgery
asbestosis
diffuse pulmonary interstitial fibrosis caused by inhaled asbestos fibers
asbestosis increases the risk of
meseothelioma
bronchogenic carcinoma
asbestosis histo and gross
ferruginous bodies in lung (asbestos fibers covered with hemosiderin)
ivory white pleural plaques
asbestosis location
lower lobes
coal workers lung affects what part of lungs
upper lobes
asbestosis professions
shipbuilders
roofers
plumbers
absent/dec breath sounds
dec resonance
dec fremitus (99)
trachea deviates towards lesion
bronchial obstruction
dec breath sounds
dull resonance
dec fremitus (99)
no tracheal deviation
pleural effusion
may have bronchial breath sounds
dull resonance
inc fremitus (99)- why?
no tracheal deviation
pneumonia (lobar)
inc fremitus due to inc vibration over consolidation
dec breath sounds
hyperresonant
absent fremitus
trachea deviates away from lesion
tension pneumothorax
leading cause of cancer death
lung
lung cancer presentation
cough
hemoptysis
bronchial obstruction
wheezing
pneumonic coin lesion on x ray
presentation:
1) mets to lung
vs
2) primary lung cancer
1) dyspnea
vs
2) cough
SPHERE of complications of lung ca
superior vena cava syndrome
pancoasts tumor
horners
endocrine
recurrent laryngeal
effusions
central location
cancer?
squamous
small cell
peripheral location
cancer?
adenocarcinoma
large cell
hilar mass arising from bronchus
cavitation
squamous cell ca
ca linked to smoking
squamous
parathyroid like activity
squamous cell ca
keratin pearls
sq cell ca
intracellular bridges
sq cell ca
Non smokers lung ca
bronchioalveolar adenocarcinoma
develops in site of prior pulmonary inflammation or injury
adenocarcinoma
most common lung ca in females
adenocarcinoma
cancer that grows along airways and can present like pneumonia
adenocarcinoma
clara cells
type II pneumos
glandular
cancer?
adenocarcinoma
aggressive undifferentiated cancer
small cell
ADH or ACTH producing cancer
small cell
cancer that may lead to Lambert Eaton
small cell
neoplasm of neuroendocrine Kulchitsky cells (small, dark blue)
small cell
cancer that doesnt respond to chemo
large cell
highly anaplastic undifferentiated cancer with poor prognosis,
removed with surgery
large cell
pleomorphic giant cells with leukocyte fragments in cytoplasm
large cell
cancer that secretes serotonin
carcinoid syndrome
carcinoid symptoms
flushing
diarrhea
wheezing
salivation
mets from what organs to lung
brain
bone
liver
pancoast tumor
carcinoma in apex of lung
affects cervical plexus
causes horners
carcinoma in apex of lung
affects cervical plexus
causes horners
pancoasts
intra alveolar exudate
consolidation
may involve entire lung
lobar pneumonia
acute inflammatory infiltrates from bronchioles into adjacent alveoli
patchy
1 or more lobes
bronchopneumonia
diffuse patchy infiltrate
localized to interstitial areas at alveolar walls
1 or more lobes
interstitial (atypical) pneumonia
localized collection of pus within parenchyma, resulting from bronchial obstruction or aspiration
lung abscess
lung abscess organisms
staph
fusiform
bacteriodes
peptostreptococcus
transudate
pleural effusion with dec protein content
transudate is caused by
CHF
nephrotic syndrome
hepatic cirrhosis
exudate
pleural effusion with inc protein content, cloudy
exudate is caused by
malignancy
pneumonia
collagen vascular disease
trauma
(states of inc vasc perm)
milky pleural effusion
inc triglycerides
lymphatic effusion
H1 blockers
reversible inhibitors of H1 histamine receptors
1st gen H1 blockers
diphenhydramine
dimenhydrinate
chlorpheniramine
diphenhydramine
1st gen H1 blocker
dimenhydrinate
1st gen H1 blocker
chlorpheniramine
1st gen H1 blocker
1st gen H1 blockers use
allergy
motion sickness
sleep aid
1st gen H1 blocker toxicity
sedation
anti muscarinic
anti alpha adrenergic
2nd gen H1 blockers
loratadine
fexofenadine
desloratadine
cetirizine
2nd gen H1 blocker use
allergy
2nd gen H1 blocker toxicity
far less sedating
dec entry into CNS
loratadine
2nd gen H1 blocker
fexofenadine
2nd gen H1 blocker
desloratadine
2nd gen H1 blocker
cetirizine
2nd gen H1 blocker
-dine, zine
2nd gen H1 blocker
bronchoconstriction is mediated by what 2 pathways
1) inflammatory
2) sympathetic tone
asthma drugs- general categories (7)
non selective beta agonists
beta 2 agonists
methylxanthines
muscarinic antagonists
cromolyn
corticosteroids
antileukotrienes
isoproterenol
nonspecific beta agonist
relaxes smooth muscle
adverse tachycardia effects
nonselective beta ag used for asthma
isoproterenol
beta 2 ags used for asthma
albuterol
salmeterol
albuterol
asthma-acute
beta 2 ag
relexes smooth muscle
salmeterol
asthma
long acting
beta 2 ag
salmeterol side effects
tremor
arrhythmia
formoterol
asthma
beta 2 ag
long term use
use beta 2 agonist long term agents for asthma with what in order to decrease toxic effects
inhaled corticosteroids
methylxanthine used for asthma
theophylline
theophylline
for asthma
a methylxanthine
bronchodilation by inhibiting phosphodeiesterase, dec cAMP hydrolysis
bronchodilation by inhibiting phosphodeiesterase, dec cAMP hydrolysis
theophylline (methylxanthine)
theophylline tox
cardio
neuro
met by P450
muscarinic antagonist used for asthma
ipratropium
tiotropium
ipratropium
muscarinic antagonist for asthma
blocks musc receptors
prevents bronchoconstriction
also used for COPD
cromolyn
asthma prophylaxis
prevents release of mediators from mast cells
corticosteroids used for asthma
beclomethasone
prednisone
corticosteroid mech for asthma treatment
inhibits NF-KB, the transcription factor that induces TNFa
antileukotrienes for asthma
zileuton
zafirukast
montelukast
zileuton mech
5 LPO inhibitor
blocks arachidonic acid conversion to leukotrienes
zafirlukast, montelukast
mechanism
block leukotrienes receptors
expectorants
guaifenesin
N-acetylcysteine
Guaifenesin mech
removes excess sputum but large doses necessary
does not suppress cough reflex
N-acetylcysteine mech
mucolytic-> loosen mucous plugs in CF
hypoxemia due to what increases A-a gradient
pulmonary causes
hypoxemia due to what causes normal A-a gradient
extrapulmonary causes
high Aa gradient values
greater than or equal to 30 mmHg
A-a gradient inc with
age
example of ventilation defect
airway collapse due to respiratory distress syndrome
example of perfusion defect
PE
example of diffusion defect
interstitial fibrosis
pulmonary edema
cardiac prob that can cause inc A-a gradient
R to L shunt
dyspnea is due to
stimulation of J receptors causing decrease in full inspiration
causes of dyspnea (4 mechs)
decreased compliance (interst fib)
inc airway resistance (chronic bronc)
chest bellows disease (obesity)
interstitial inflamm/fluid (left HF)
cough receptors are
located at bifurcations of airways, larynx, distal esophagus
cough with normal chest xray
postnasal discharge is most common
productive cough: 3
chronic bronch- cigarettes
typical bacterial pneum
bronchiectasis
hemoptysis causes: 6
chronic bronchitis- most common
pneumonia
bronch carcinoma
TB
bronchiectasis
aspergillas
normal resp rate
14-20 bpm
normal resp rate is up to what in kids
44 bpm
tachypnea: how many bpm?
greater than 20
causes of tachypnea:3
restrictive lung disease
pleuritic chest pain
PE with infarction
tracheal shift mechanism
due to large changes in pleural fluid volume
causes of tracheal shift
large tension pneumo
large pleural effusion
large spontaneous pneumo
vocal tactile fremitus
palpable thrill (vibration) transmitted thru chest when patient says E, 123, or 99
decreased fremitus causes:
emphysema
asthma
(inc AP with inc in TLC)
absent fremitus causes:
atelectasis (airway collapse)
fluid
air (pneumothorax) in pleural space
increased fremitus:
alveolar consolidation (lobar pneum)
dull percussion:
pleural effusion
lung consolidation
atelectasis (no air in alveoli)
hyperresonant percussion with
pneumothorax
asthma
emphysema
effects of inflammation in small airways (cb, asthma)
air trapping
wheezing
inc airway resistance
bronchial breath sounds
always abnormal
loud high pitched
due to consolidation
(bronchi are patent and partially collapsed)
crackles
usually inspiratory
early to midinspiratory crackles
secretions in large to mid airways
late insp crackles
interstitial fluid- due to reopening of distal airways partially occluded by interstitial pressure (CHF)
wheezing
high pitched
expiration
due to inflam (asthma, CB)
due to pulmonary edema or infarct
inspiratory sound
crackles
expiratory sound
wheezing
ronchi
low pitched snoring sound
insp or exp
secretions in large airways
Chronic bronchitis
inspiratory stridor
high pitched inspiratory sound
upper airway obstruction (epiglottitis or croup)
insp and exp stridor
sign of fixed airway obstruction (cancer)
causes of pleuritis
cancer
infarct
pneumonia
SLE serositis
grunting in newborns
always abnormal after 24 hrs
common in RDS
hypoxemia + normal A-a:
3 mech
depress resp center
upper airway obstruction
chest bellows disease
chest bellows (muscles of respiration) disease
paralyzed diaphragm
ALS
spirometry does not measure
FRC
TLC
RV
FVC
total air expelled after max inspiration
5 L
FEV1sec
forced exp volume in 1 sec
4L
normal FVC/FEV1
80%
5L/4L
end of max inspiration
TLC
end of max expiration
RV
nonuniform emptying
expiratory curve shifts to left
obstructive
exp curve shifts to right
restrictive
choanal atresia
newborn cant breathe through nose
cyanosis while breast feeding
unilateral or bilateral bony septum between nose and pharynx
most common cause of nasal polyp
allergic polyp
patient that takes aspirin and has nasal polyp
asthma patient
nasal polyps in child
CF
obstructive sleep apnea pathogenesis
airway obstruction causes CO2 retention, leading to hypoxemia
dec what during apneic episodes
PO2
O2 sat
inc in PCO2
is resp acidosis
complications of obst sleep apnea
pulm htn leading to RVH
(cor pulmonale)
secondary polycythemia (hypoxia stim erythro)
sinus infection location in adult
maxillary
sinus infection location in kid, and most common cause
ethmoid
viral URI
diabetics commonly have sinusitis due to
mucor
nasopharyngeal carcinoma (squamous)
men
china
africa
EBV
laryngeal cancer
smoking
alcohol
squamous papillomas 6 and 11
atelectasis
loss of lung volume due to inadequate expansion of airspaces
most common cause of fever 24 to 36 hrs after surgery
resporption atelectasis (airway obstruction due to thick secretions)
resporption atelectasis: mech of alveolar collapse
lack of air and distal resorption of preexisting air through pores of kohn in alveolar walls
absent vibratory sensation
dullness to percussion
absent breath sounds
resorption atelectasis
compression atelectasis
air under pressure or fluid in pleural cavity:
tension pneumo or pleural effusion
surfactant is stored in
lamellar bodies
synthesis of surfactant begins
in 28th week of gestation
synthesis of surfactant is inc with
cortisol
thyroxine
synth of surfactant is dec with
insulin
maternal diabetes causes RDS: mech
fetal hyperglycemia inc insulin release, insulin dec surfactant synthesis
C section causes RDS: mech
lack of stress induced cortisol release, cortisol inc surfactant synthesis
widespread atelectasis (from RDS) results in
massive intrapulmonary shunting (perfusion but no ventilation)
newborn with:
grunting
tachypnea
intercostal retractions
RDS
infants with RDS dev
hypoxemia and resp acidosis
RDS complications
blindness from O2 therapy ROS
bronchopulmonary dysplasia
PDA
necrotizing enterocolitis (gut ischemia)
hypoglycemia
most common cause of pulm edema
left sided heart failure
edema due to alterations in starling pressure
transudate
(CHF, nephrotic syndr, cirrhosis)
edema due to microvascular or alveolar injury
exudate
(sepsis, pneumonia, aspiration, drugs, high altitude, ARDS)
ARDS mech
damage to alveolar walls->
macs release cytokines->
cytokines attract neutrophils-> damage capillaries and cause protein leak and hyaline membrane
damage to alveolar walls->
macs release cytokines->
cytokines attract neutrophils-> damage capillaries and cause protein leak and hyaline membrane
ARDS mech
severe hypoxemia not responsive to O2 therapy
ARDS
PaO2 < 50 mmHg
pulm artery wedge < 18
ARDS
interstitial pneumonia, no signs of consolidation
atypical pneumonia
TB resides where
in phagosomes of alveolar macs
produces protein that prevents fusion of lysosomes with phagosome
produces protein that prevents fusion of lysosomes with phagosome of alveolar macs
TB
cord factor is virulence factor
TB
responsible for positive PPD
protein in cell wall
TB drug resistance mech
mutations involving mycolic acid
mutations involving catalase peroxidase
enzyme required to activate isoniazid
catalase peroxidase
primary TB location
upper part of lower lobes
secondary TB location
lower part of upper lobes
Ghon focus
caseous necrosis in periphery
Ghon complex
caseous necrosis in hilar lymph nodes
cavitary lesion of TB is due to
release of cytokines from memory T cells
fever
night sweats
wt loss
TB
miliary TB spread: extrapulmonary sites
kidney is most common (via pulmonary veins)
adrenal--> addisons
tx TB
isoniazid
rifampin
pyrazinamide
when do you become noninfectious with TB tx
2-3 weeks (keep treating for 9-12 mo)
TB in vertebra
Potts disease
tx MAC
clarithromycin
rifabutin
ethambutol
lung abscess most common cause
aspiration of oropharyngeal material
risk factors of lung absess
alc
loss of consc
recent dental work
spiking fever with productive foul smelling cough
lung abscess
most common site of aspiration
superior right lower lobe
tx lung abscess
clindamycin
majority of PEs come from
femoral
consequences of pulmonary artery occlusion
inc in pulmonary artery pressure
dec blood flow to pulm parenchyma-> hemorrhagic infarct
bronchial arteries arise from
intercostals
aorta
acute right ventricular strain and sudden death
saddle embolus
dyspnea and tachypnea most common
respiratory alkalosis
hypoxemia
fever
pleurtic pain
pulmonary infarct
pulm infarct expiratory wheezing mech
release of TXA2 from platelets
PCO2 < 30
PO2 < 80
inc in A-a gradient
inc in D dimers
PE
cut off sign of one or more pulmonary arteries on CXR
PE
hamptons hump
wedge shaped area of consolidation due to PE
normal Ventilation scan
abnormal perfusion scan
PE
main cause of secondary pulm htn
respiratory acidosis and hypoxemia
vascular hyperreactivity with proliferation of smooth muscle
primary pulm htn
mutations in genes assoc with transforming growth factor beta
primary pulm htn
secondary pulm htn mech
endothelial cell dysfunction
loss of vasodilators NO
inc in vasoconstrictors endothelin
hypoxemia and resp acidosis result
causes smooth muscle hyper
5 general categories of mech causing secondary pulm htn
chronic hypoxemia- high alt
chronic resp acidosis- CB, OSA
loss of pulm vasc
left to right shunt
mitral stenosis
atherosclerosis of main elastic pulm arteries
pulm htn
exertional dyspnea
chest pain
tapering pulm arteries on cxr
accentuated P2
pulm htn
left parasternal heave
sign of right ventricle hypertrophy
pulm htn imposes what on right ventricle
inc afterload
tx pulm htn
diuretics
oxygen
vasodilators
earliest manifestation of interstitial fibrosis
alveolitis
leukocytes release cytokines, which stimulate fibrosis, causing
interstitial fibrosis
dec lung compliance
dec expansion of lung parenchyma
inc lung elasticity (recoil on expiration)
interstitial fibrosis
CWP: anthracotic pigment where
alveolar macs (dust cells) in interstitial tissue and hilar lymph nodes
dust cells
coal workers pneum.
coal deposits next to respiratory bronchioles cause
centriacinar emphysema
black lung disease
complicated coal workers pneum:
progressive massive fibrosis
caplan syndrome
pneumoconiosis and cavitating rheumatoid nodules
most common occupational disease
silicosis
silicosis mech
quartz in macs stimulates cytokines that stim fibrosis
ground glass cxr
silicosis
egg shell calcification in hilar nodes
silicosis
inc risk of lung cancer and TB with
silicosis (not coal workers pneum)
amphibole
straight asbestos fibers
produce interstitial fibrosis, mesothelioma, lung cancer
asbestos fibers deposit where
respiratory unit: resp bronch, alveolar ducts, alveoli
benign pleural plaques
most common lesion of asbestosis
most common asbestos related cancer
primary bronchogenic carcinoma
cancer arising from serosa of pleura
no assoc with smoking
encases lung
20-40 yrs after exposure
mesothelioma (asbestosis)
berylliosis
exposure to nuclear and aerospace industry
interstitial fibrosis, noncase granulomas
cor pulmonale and lung ca risk
sarcoidosis- what is it and epi
multisystem granulomatous disease
blacks
women
nonsmokers
sarcoid pathogenesis
disorder in immune regulation
CD4 T cells react with unknown antigen
release cytokines-> granulomas
disorder in immune regulation
CD4 T cells react with unknown antigen
release cytokines-> granulomas
sarcoid
sarcoid granulomas location
interstitium
mediastinal LNs
hilar LNs
granulomas with multinuc giant cells
sarcoid
schaumann bodies (laminated calcium concretions)
sarcoid
stellate inclusions/asteroid bodies
sarcoid
most common symptom of sarcoidosis
dyspnea
sarcoidosis organ involvement
lung
skin nodules
eye lesions/uveitis
liver lesions
enlarged glands
hypothal and pituitary
bone marrow
spleen
inc ACE
sarcoidosis
hypercalcemia due to inc synth of 1 alpha OH
sarcoidosis
tx sarcoid
most have spontaneous remission
corticosteroids
idiopathic pulmonary fibrosis
alveolitis leading to interstitial fibrosis
honeycomb lung
IPF
IPF epi
males
40-70
IPF pathogenesis
repeated cycles of alveolitis triggered by unknown agent
release cytokines-> fibrosis-> proximal dilation of small airways
repeated cycles of alveolitis triggered by unknown agent
release cytokines-> fibrosis-> proximal dilation of small airways
IPF pathogenesis
fever
dyspnea with exertion
chronic nonprod cough
late insp crackles
IPF
collagen vascular disease with interstitial fibrosis
SLE
RA
pleural effusion in young woman
SLE
pulmonary findings in RA
rheum nodules
interstitial fibrosis
hypersensitivity pneumonitis
extrinsic allergic alveolitis
known antigen
No IgE or esoinophilia
types of hypersens pneumonia
farmers lung
silo fillers disease
byssinosis
farmers lung
thermophilic actinomycetes in moldy hay

IgG antibodies and antigen form immune complexes
farmers lung hypersensitivity
acute is type 3 (IgG + antigen)
chronic is type 4- develop granulomas
inhale gases from plant material
(oxides of nitrogen)
silo fillers disease
dyspnea with contact with cotton, linen, hemp products-> monday morning blues
byssinosis
interstitial fibrosis drugs
bleomycin
amiodarone
cyclophosph
methotrexate
methysergide
nitrosourea
nitrofurantoin
emphysema targets what
respiratory unit (permanent enlargement of all or part)
increased compliance
decreased elasticity
emphysema
pathogenesis of emphysema
elastase and oxidants derive from neutrophils and macs--> destroy elastic tissue
how does cigarette smoke cause emphysema?
cigs are chemotactic to neuts,
inactivate alpha 1 antitrypsin and glutathione via free radicals and elastases
destruction of elastic tissue (emphysema) causes
loss of radial traction-> small airways collapse on expiration
destruction of distal terminal bronchioles and RBs, apical segments of upper lobe:
centriacinar emphysema
Genetics of AAT deficiency
AD
MM phenotype is normal
homozygous ZZ has decreased AAT synth by liver
distal terminal bronchioles and entire respiratory unit, lower lobes
panacinar emphysema (AAT def)
absent alpha 1 globulin peak in serum protein electrophoresis
AAT def
breath sounds diminished due to hyperinflation
cxr- hyperlucency, inc AP, depressed diaphragms
emphysema
targets alveolar ducts and alveoli
subpleural
paraseptal emphysema
cyanosis of skin and mucous membranes
-due to dec O2 sat (hypoxemia)
chronic bronchitis
arterial PCO2 > 45
bicarb > 30
chronic bronchitis
loss of ciliated epithelium and presence of squamous metaplasia
chronic bronchitis
turbulent airflow occurs in
bronchi
laminar airflow occurs in
terminal bronchioles
emphysema PCO2
normal to decreased
chronic bronch PCO2
inc
chronic bronch pH
dec
emphysema pH
normal to inc
cor pulmonale is common consequence of what obstructive airway disease
chronic bronchitis
onset of hypoxemia in emphysema
late
onset of hypoxemia in chronic bronch
early
onset of dyspnea in emphysema
early
onset of dyspnea in chronic bronch
late
IL4
isotype switching to IgE
isotype switching to IgE
IL4
IL5
production and activation of eosinophils
production and activation of eosinophils
IL5
asthma- helper T cells release what
IL4-> IgE
IL5- eosinophils
inhaled antigens in asthma cross link what
IgE on mast cells-> histamine release
late phase reaction of asthma
eotaxin is produced- chemotactic for eosinophils
in asthma, what do eosinophils produce
major basic protein and cationic protein which damage epithelial cells and constrict airway
eotaxin
chemotactic for eosinophils
patchy loss of epithelial cells
goblet metaplasia
thick BM
smooth muscle hypertrophy
asthma
expiratory wheeze
nocturnal cough
initial alkalosis
inc AP due to air trapping
asthma
indicates need for intubation in bronchial asthma
normal pH or resp acidosis
O3
free radical
from O2 + oxides of nitrogen or sulfur
(ozone)
can cause asthma
4 causes of bronchiectasis
CF
infections- TB
bronchial obstruction
primary ciliary dyskinesia
sputum
hemoptysis
digital clubbing
cor pulmonale
bronchiectasis
CF pathogenesis
defective CF transmembrane conductance regulator CFTR for chloride ions,
CFTR is degraded in golgi-->
dec Na and Cl reabsorption
lung cancer is declining in __ and increasing in __
decline in men
inc in women
most lung cancers are
non small cell (87%)
most common site of lunc ca mets
hilar LNs
solitary pulm nodule is most often
granuloma (peripheral coin lesion)
most common met to lung
breast (then colon and renal)
scar carcinoma- dev in old scar
adenocarcinoma
carcinoma that tends to cavitate
squamous
cancer with no relation to smoking
adenocarcinoma and large cell
most common primary lung tumor in kids
carcinoid
bronchial hamartoma
cartilage
adipose
solitary coin lesion
popcorn calcification
cartilage
adipose
solitary coin lesion
popcorn calcification
bronchial hamartoma
mediastinal mass in older patient
metastatic lung ca
mediastinal mass in young patient
primary disease
most common primary mediastinal mass
neurogenic tumor- usually benign in adults, malignant in kids
most common site for mediastinal mass
anterior compartment
malignant mediastinal mass in kids
neuroblastoma
benign mediastinal mass in adult
ganglioneuroma
neurogenic tumors location
posterior mediastinum
5 masses of mediastinum
neurogenic tumor
thymoma
pericardial cyst
malignant lymphoma
teratoma
middle mediastinum mass
pericardial cyst
anterior mediastinal mass in younger woman
lymphoma
benign cystic mass in anterior mediastinum
teratoma
thymoma location
anterior mediastinum
benign
thymoma is made up of
epithelium
(not lymphoid tissue)
thymomas are associated with
myasthenia gravis (Ach receptor antibodies)
associated with:
hypogammaglobulinemia
pure RBC aplasia
autoimmune diseases
thymoma
most common cause of pleural effusion
CHF
most common cause of pleural exudate
TB and malignancy
chylous pleural effusion
blockage of thoracic duct
due to malig or trauma
milky turbid appearance
chylomicrons form supranate
pesudochylous effusion
RA (inc in cholesterol caused by inflammation)
transudate pH
> 7.4
exudate pH
< 7.4
large effusion shift
contralateral shift
subpleural blebs secondary to
high negative intrapleural pressures
shift:
spontaneous vs tension pneumo
spontaneous: trachea towards side of collapse

tension: trachea to contralat side
tension pneumo
trauma to lungs
inc in pleural cavity pressure with each breath